TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Obradović, Milan
AU  - Jovanovic, Aleksandra
AU  - Popović-Đorđević, Jelena
AU  - Dobutović, Branislava
AU  - Jevremovic, Danimir
AU  - Marche, Pierre
AU  - Isenovic, Esma R.
PY  - 2014
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/1853
AB  - In this study, the role of epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK1/2), heparin-binding EGF-like growth factor (HB-EGF), general metalloproteinases, matrix metalloproteinases-2 (MMP-2) in mediating the mitogenic action of thrombin in rat vascular smooth muscle cells (VSMC) was investigated. The incubation of rat VSMC with thrombin (1 U/ml) for 5 min resulted in significant (p  lt  0.001) increase of ERK1/2 phosphorylation by 8.7 +/- A 0.9-fold, EGFR phosphorylation by 8.5 +/- A 1.3-fold (p  lt  0.001) and DNA synthesis by 3.6 +/- A 0.4-fold (p  lt  0.001). Separate 30-min pretreatments with EGFR tyrosine kinase irreversible inhibitor, 10 A mu M PD169540 (PD), and 20 A mu M anti-HB-EGF antibody significantly reduced thrombin-stimulated EGFR and ERK1/2 phosphorylation by 81, 72 % and by 48 and 61 %, respectively. Furthermore, the same pretreatments with PD or anti-HB-EGF antibody reduced thrombin-induced VSMC proliferation by 44 and 45 %, respectively. In addition, 30-min pretreatments with 10 A mu M specific MMP-2 inhibitor significantly reduced thrombin-stimulated phosphorylation of both EGFR and ERK1/2 by 25 %. Moreover, the same pretreatment with MMP-2 inhibitor reduced thrombin-induced VSMC proliferation by 45 %. These results show that the thrombin-induced DNA synthesis correlates with the level of ERK1/2 activation rather than EGFR activation. These results further suggest that thrombin acts through EGFR and ERK 1/2 signaling pathways involving MMP-2 to upregulate proliferation of VSMC.
PB  - Springer, Dordrecht
T2  - Molecular and Cellular Biochemistry
T1  - Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2
VL  - 396
IS  - 1-2
SP  - 147
EP  - 160
DO  - 10.1007/s11010-014-2151-y
ER  - 

@article{
author = "Smiljanić, Katarina and Obradović, Milan and Jovanovic, Aleksandra and Popović-Đorđević, Jelena and Dobutović, Branislava and Jevremovic, Danimir and Marche, Pierre and Isenovic, Esma R.",
year = "2014",
abstract = "In this study, the role of epidermal growth factor receptor (EGFR), extracellular signal-regulated kinase (ERK1/2), heparin-binding EGF-like growth factor (HB-EGF), general metalloproteinases, matrix metalloproteinases-2 (MMP-2) in mediating the mitogenic action of thrombin in rat vascular smooth muscle cells (VSMC) was investigated. The incubation of rat VSMC with thrombin (1 U/ml) for 5 min resulted in significant (p  lt  0.001) increase of ERK1/2 phosphorylation by 8.7 +/- A 0.9-fold, EGFR phosphorylation by 8.5 +/- A 1.3-fold (p  lt  0.001) and DNA synthesis by 3.6 +/- A 0.4-fold (p  lt  0.001). Separate 30-min pretreatments with EGFR tyrosine kinase irreversible inhibitor, 10 A mu M PD169540 (PD), and 20 A mu M anti-HB-EGF antibody significantly reduced thrombin-stimulated EGFR and ERK1/2 phosphorylation by 81, 72 % and by 48 and 61 %, respectively. Furthermore, the same pretreatments with PD or anti-HB-EGF antibody reduced thrombin-induced VSMC proliferation by 44 and 45 %, respectively. In addition, 30-min pretreatments with 10 A mu M specific MMP-2 inhibitor significantly reduced thrombin-stimulated phosphorylation of both EGFR and ERK1/2 by 25 %. Moreover, the same pretreatment with MMP-2 inhibitor reduced thrombin-induced VSMC proliferation by 45 %. These results show that the thrombin-induced DNA synthesis correlates with the level of ERK1/2 activation rather than EGFR activation. These results further suggest that thrombin acts through EGFR and ERK 1/2 signaling pathways involving MMP-2 to upregulate proliferation of VSMC.",
publisher = "Springer, Dordrecht",
journal = "Molecular and Cellular Biochemistry",
title = "Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2",
volume = "396",
number = "1-2",
pages = "147-160",
doi = "10.1007/s11010-014-2151-y"
}

Smiljanić, K., Obradović, M., Jovanovic, A., Popović-Đorđević, J., Dobutović, B., Jevremovic, D., Marche, P.,& Isenovic, E. R.. (2014). Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2. in Molecular and Cellular Biochemistry
Springer, Dordrecht., 396(1-2), 147-160.
https://doi.org/10.1007/s11010-014-2151-y

Smiljanić K, Obradović M, Jovanovic A, Popović-Đorđević J, Dobutović B, Jevremovic D, Marche P, Isenovic ER. Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2. in Molecular and Cellular Biochemistry. 2014;396(1-2):147-160.
doi:10.1007/s11010-014-2151-y .

Smiljanić, Katarina, Obradović, Milan, Jovanovic, Aleksandra, Popović-Đorđević, Jelena, Dobutović, Branislava, Jevremovic, Danimir, Marche, Pierre, Isenovic, Esma R., "Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2" in Molecular and Cellular Biochemistry, 396, no. 1-2 (2014):147-160,
https://doi.org/10.1007/s11010-014-2151-y . .

TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Resanović, I.
AU  - Savić, Kristina
AU  - Jovanović, A.
AU  - Zafirović, S.
AU  - Obradović, Milan
AU  - Isenović, E. R.
PY  - 2013
UR  - http://cherry.chem.bg.ac.rs/handle/123456789/6449
AB  - Zajednički činilac u nastanku vaskularnih oboljenja kao što su ateroskleroza, restenoza i hipertenzija je patološka proliferacija i akumulacija glatkih mišićnih ćelija krvnog suda (VSMC) u njegov unutrašnji (intima) sloj.  Trombin, ključni hormon koagulacionoaterogenetske mreže posreduje u regulisanju tonusa i propustljivosti krvnih sudova, migracije i proliferacije VSMC, privlačenja monocita i raznih proinflamatornih markera u aterosklerotske lezije i svoje efekte ostvaruje direktno kao serinska proteinaza i aktivacijom svojih receptora spregnutih sa G proteinom (GPCR). Pokazano je da trombin posreduje u proliferaciji VSMC transaktivacijom receptora za epidermalni faktor rasta (EGFR). Proces transaktivacije EGFR preko aktivacije trombinskih receptora, uključuje metaloproteinaze koje generišu ligande proteolitičkim cepanjem membranskih prekursora, kao što je heparin vezujući epidermalni faktor rasta (HB-EGF) koji se vezuje za EGFR i aktivira ga, što vodi proliferaciji VSMC preko nishodnih, signalnih puteva mitogenom aktiviranih protein kinaza (MAPK).  U okviru ovog preglednog članka su prikazani i diskutovani novi literaturni podaci koji se odnose na: ulogu aktivacije EGFR u posredovanju proliferativnog efekta trombina na VSMC, razumevanje i reviziju koncepta trostruke kaskade transaktivacije EGFR stimulisane trombinom u mehanizmu proliferacije VSMC.
AB  - The common factor in the development of
vascular diseases, such as atherosclerosis,
hypertension and restenosis, is excessive accumulation
and proliferation of vascular smooth muscle cells
(VSMC) within inner (intima) layer of vessel wall.
 Thrombin, a key player in athero-coagulation
maze, mediates the regulation of vascular permeability
and contraction, migration and proliferation of VSMC,
attracting monocytes and a variety of proinflammatory markers in atherosclerotic lesions.
Thrombin exerts its effects either directly as serine
proteinases and/or via activation of its G proteins
coupled receptors (GPCR). It has been shown that
thrombin mediates transactivation of epidermal growth
factor receptor (EGFR) within the process of VSMC
proliferation. EGFR transactivation process through
the activation of thrombin protease activated receptor
(PAR), includes a matrix metalloproteinase cleavage of
membrane ligands precursors such as epidermal
growth factor like growth factor that binds heparin
(HB-EGF) that binds to the EGFR and activates it,
leading to VSMC proliferation via downstream
signaling pathways of mitogen activated protein kinase
(MAPK).
 This review article presents review of the new
literature data concerning: the role of EGFR
activation in mediating the proliferative effect of
thrombin in VSMC and understanding of the concept of
the triple cascade of EGFR transactivation stimulated
by thrombin in the mechanism of VSMC proliferation.
PB  - Univerzitet u Beogradu - Medicinski fakultet
T2  - Medicinska Istraživanja
T1  - Role of the epidermal growth factor receptor in thrombin regulated vascular smooth muscle cells proliferation
T1  - Uloga receptora za epidermalni faktor rasta u trombinom regulisanoj proliferaciji glatkih mišićnih ćelija krvnih sudova
VL  - 47
IS  - 1
SP  - 10
EP  - 20
DO  - 10.5937/MedIst1301005S
ER  - 

@article{
author = "Smiljanić, Katarina and Resanović, I. and Savić, Kristina and Jovanović, A. and Zafirović, S. and Obradović, Milan and Isenović, E. R.",
year = "2013",
abstract = "Zajednički činilac u nastanku vaskularnih oboljenja kao što su ateroskleroza, restenoza i hipertenzija je patološka proliferacija i akumulacija glatkih mišićnih ćelija krvnog suda (VSMC) u njegov unutrašnji (intima) sloj.  Trombin, ključni hormon koagulacionoaterogenetske mreže posreduje u regulisanju tonusa i propustljivosti krvnih sudova, migracije i proliferacije VSMC, privlačenja monocita i raznih proinflamatornih markera u aterosklerotske lezije i svoje efekte ostvaruje direktno kao serinska proteinaza i aktivacijom svojih receptora spregnutih sa G proteinom (GPCR). Pokazano je da trombin posreduje u proliferaciji VSMC transaktivacijom receptora za epidermalni faktor rasta (EGFR). Proces transaktivacije EGFR preko aktivacije trombinskih receptora, uključuje metaloproteinaze koje generišu ligande proteolitičkim cepanjem membranskih prekursora, kao što je heparin vezujući epidermalni faktor rasta (HB-EGF) koji se vezuje za EGFR i aktivira ga, što vodi proliferaciji VSMC preko nishodnih, signalnih puteva mitogenom aktiviranih protein kinaza (MAPK).  U okviru ovog preglednog članka su prikazani i diskutovani novi literaturni podaci koji se odnose na: ulogu aktivacije EGFR u posredovanju proliferativnog efekta trombina na VSMC, razumevanje i reviziju koncepta trostruke kaskade transaktivacije EGFR stimulisane trombinom u mehanizmu proliferacije VSMC., The common factor in the development of
vascular diseases, such as atherosclerosis,
hypertension and restenosis, is excessive accumulation
and proliferation of vascular smooth muscle cells
(VSMC) within inner (intima) layer of vessel wall.
 Thrombin, a key player in athero-coagulation
maze, mediates the regulation of vascular permeability
and contraction, migration and proliferation of VSMC,
attracting monocytes and a variety of proinflammatory markers in atherosclerotic lesions.
Thrombin exerts its effects either directly as serine
proteinases and/or via activation of its G proteins
coupled receptors (GPCR). It has been shown that
thrombin mediates transactivation of epidermal growth
factor receptor (EGFR) within the process of VSMC
proliferation. EGFR transactivation process through
the activation of thrombin protease activated receptor
(PAR), includes a matrix metalloproteinase cleavage of
membrane ligands precursors such as epidermal
growth factor like growth factor that binds heparin
(HB-EGF) that binds to the EGFR and activates it,
leading to VSMC proliferation via downstream
signaling pathways of mitogen activated protein kinase
(MAPK).
 This review article presents review of the new
literature data concerning: the role of EGFR
activation in mediating the proliferative effect of
thrombin in VSMC and understanding of the concept of
the triple cascade of EGFR transactivation stimulated
by thrombin in the mechanism of VSMC proliferation.",
publisher = "Univerzitet u Beogradu - Medicinski fakultet",
journal = "Medicinska Istraživanja",
title = "Role of the epidermal growth factor receptor in thrombin regulated vascular smooth muscle cells proliferation, Uloga receptora za epidermalni faktor rasta u trombinom regulisanoj proliferaciji glatkih mišićnih ćelija krvnih sudova",
volume = "47",
number = "1",
pages = "10-20",
doi = "10.5937/MedIst1301005S"
}

Smiljanić, K., Resanović, I., Savić, K., Jovanović, A., Zafirović, S., Obradović, M.,& Isenović, E. R.. (2013). Role of the epidermal growth factor receptor in thrombin regulated vascular smooth muscle cells proliferation. in Medicinska Istraživanja
Univerzitet u Beogradu - Medicinski fakultet., 47(1), 10-20.
https://doi.org/10.5937/MedIst1301005S

Smiljanić K, Resanović I, Savić K, Jovanović A, Zafirović S, Obradović M, Isenović ER. Role of the epidermal growth factor receptor in thrombin regulated vascular smooth muscle cells proliferation. in Medicinska Istraživanja. 2013;47(1):10-20.
doi:10.5937/MedIst1301005S .

Smiljanić, Katarina, Resanović, I., Savić, Kristina, Jovanović, A., Zafirović, S., Obradović, Milan, Isenović, E. R., "Role of the epidermal growth factor receptor in thrombin regulated vascular smooth muscle cells proliferation" in Medicinska Istraživanja, 47, no. 1 (2013):10-20,
https://doi.org/10.5937/MedIst1301005S . .

TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Savić, Kristina
AU  - Obradovic, Milan
AU  - Putniković, Biljana
AU  - Đorđević, Jelena
AU  - Isenović, Esma
PY  - 2013
UR  - http://cherry.chem.bg.ac.rs/handle/123456789/6448
AB  - Kardiovaskularne bolesti predstavljaju najveći uzrok smrtnosti ljudske populacije, a jedna od njihovih najučestalijih patoloških komponenti je i sama ateroskleroza. Proliferacija ili deoba glatkih mišićnih ćelija krvnih sudova (VSMC) ključni je događaj u nastanku raznih vaskularnih oboljenja, uključujući aterosklerozu i hipertenziju. U procesu diferencijacije i abnormalne deobe VSMC povezanih sa hipertenzijom i aterosklerozom uključen je i trombin. Stimulisanje VSMC trombinom dovodi do aktivacije ekstracelularnim signalima regulisanih kinaza 1 i 2 (ERK1/2), preko transaktivacije receptora za epidermalni faktor rasta (EGFR). U našim ranijim studijama potvrdili smo na osnovu inhibicije ERK1/2 od strane PD9805 inhibitora, učešće ERK1/2 u regulaciji proliferacije VSMC izazvanoj trombinom. Takođe, protein kinaza C delta (PKCδ), detektovana je u VSMC i pokazano je da je i njena aktivnost takođe regulisana trombinom. U okviru ovog preglednog članka biće prikazani literaturni podaci koji se odnose na ulogu PKCδ i ERK1/2, u posredovanju proliferativnog efekta trombina na VSMC.
AB  - Cardiovascular disease is the greatestest single
cause of mortality and its major underlying pathology
is atherosclerosis. The proliferation of vascular smooth
muscle cells (VSMC) is a key event in the pathogenesis
of various vascular diseases, including atherosclerosis
and hypertension. Thrombin is involved in the
differentiation and abnormal proliferation of VSMC
associated with atherosclerosis and hypertension.
Thrombin stimulation results in extracellular
signal-regulated kinase (ERK1/2) activation through
transactivation of the epidermal growth factor receptor
(EGFR). Based on our reacent studies in which
PD98059 used to inhibit ERK1/2, we have shown
previously that ERK1/2 was involved in the regulation
by thrombin of VSMC’s proliferation. In addition,
protein kinase C delta (PKCδ) have also been detected
in VSMC and shown to be regulated by thrombin.
In this review, we are presenting literature data
relating to role of PKCδ and ERK1/2 in mediating the
mitogenic action of thrombin in VSMC.
PB  - Univerzitet u Beogradu - Medicinski fakultet
T2  - Medicinska Istraživanja
T1  - Role Of Pkc-delta And Erk1/2 In Trombin stimulated vascular smooth muscle cells proliferation
T1  - Uloga PKCd i ERK1/2 u trombinom stimulisanoj proliferaciji glatkih mišićnih ćelija krvnih sudova
VL  - 47
IS  - 1
SP  - 5
EP  - 9
DO  - 10.5937/MedIst1301005S
ER  - 

@article{
author = "Smiljanić, Katarina and Savić, Kristina and Obradovic, Milan and Putniković, Biljana and Đorđević, Jelena and Isenović, Esma",
year = "2013",
abstract = "Kardiovaskularne bolesti predstavljaju najveći uzrok smrtnosti ljudske populacije, a jedna od njihovih najučestalijih patoloških komponenti je i sama ateroskleroza. Proliferacija ili deoba glatkih mišićnih ćelija krvnih sudova (VSMC) ključni je događaj u nastanku raznih vaskularnih oboljenja, uključujući aterosklerozu i hipertenziju. U procesu diferencijacije i abnormalne deobe VSMC povezanih sa hipertenzijom i aterosklerozom uključen je i trombin. Stimulisanje VSMC trombinom dovodi do aktivacije ekstracelularnim signalima regulisanih kinaza 1 i 2 (ERK1/2), preko transaktivacije receptora za epidermalni faktor rasta (EGFR). U našim ranijim studijama potvrdili smo na osnovu inhibicije ERK1/2 od strane PD9805 inhibitora, učešće ERK1/2 u regulaciji proliferacije VSMC izazvanoj trombinom. Takođe, protein kinaza C delta (PKCδ), detektovana je u VSMC i pokazano je da je i njena aktivnost takođe regulisana trombinom. U okviru ovog preglednog članka biće prikazani literaturni podaci koji se odnose na ulogu PKCδ i ERK1/2, u posredovanju proliferativnog efekta trombina na VSMC., Cardiovascular disease is the greatestest single
cause of mortality and its major underlying pathology
is atherosclerosis. The proliferation of vascular smooth
muscle cells (VSMC) is a key event in the pathogenesis
of various vascular diseases, including atherosclerosis
and hypertension. Thrombin is involved in the
differentiation and abnormal proliferation of VSMC
associated with atherosclerosis and hypertension.
Thrombin stimulation results in extracellular
signal-regulated kinase (ERK1/2) activation through
transactivation of the epidermal growth factor receptor
(EGFR). Based on our reacent studies in which
PD98059 used to inhibit ERK1/2, we have shown
previously that ERK1/2 was involved in the regulation
by thrombin of VSMC’s proliferation. In addition,
protein kinase C delta (PKCδ) have also been detected
in VSMC and shown to be regulated by thrombin.
In this review, we are presenting literature data
relating to role of PKCδ and ERK1/2 in mediating the
mitogenic action of thrombin in VSMC.",
publisher = "Univerzitet u Beogradu - Medicinski fakultet",
journal = "Medicinska Istraživanja",
title = "Role Of Pkc-delta And Erk1/2 In Trombin stimulated vascular smooth muscle cells proliferation, Uloga PKCd i ERK1/2 u trombinom stimulisanoj proliferaciji glatkih mišićnih ćelija krvnih sudova",
volume = "47",
number = "1",
pages = "5-9",
doi = "10.5937/MedIst1301005S"
}

Smiljanić, K., Savić, K., Obradovic, M., Putniković, B., Đorđević, J.,& Isenović, E.. (2013). Role Of Pkc-delta And Erk1/2 In Trombin stimulated vascular smooth muscle cells proliferation. in Medicinska Istraživanja
Univerzitet u Beogradu - Medicinski fakultet., 47(1), 5-9.
https://doi.org/10.5937/MedIst1301005S

Smiljanić K, Savić K, Obradovic M, Putniković B, Đorđević J, Isenović E. Role Of Pkc-delta And Erk1/2 In Trombin stimulated vascular smooth muscle cells proliferation. in Medicinska Istraživanja. 2013;47(1):5-9.
doi:10.5937/MedIst1301005S .

Smiljanić, Katarina, Savić, Kristina, Obradovic, Milan, Putniković, Biljana, Đorđević, Jelena, Isenović, Esma, "Role Of Pkc-delta And Erk1/2 In Trombin stimulated vascular smooth muscle cells proliferation" in Medicinska Istraživanja, 47, no. 1 (2013):5-9,
https://doi.org/10.5937/MedIst1301005S . .

TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Zafiroviç, Sonja
AU  - Obradovic, Milan
AU  - Gluvić, Zoran
AU  - Stokić, Edita
AU  - Putniković, Biljana
AU  - Isenović, Esma
PY  - 2012
UR  - http://cherry.chem.bg.ac.rs/handle/123456789/6442
AB  - Glatke misićne ćelije krvnih sudova
 (VSMCs) su od vitalnog znaiaja, kako za struk
turu tako i za funkcionisanje i dinamiku krvnih
 sudova. Proliferacija i abnormalna akumulacija
 VSMCs su medu kljucnim dogadajima u nastan
ku raznih vaskularnih oboljenja, ukljudujuii ate
rosklerozu i hipertenziju. Kardiovaskularne bole
sti su vodeii uzrok smrtnosti ljudske populacije u
 dijoj osnovi u najveioj meri dominira aterosklero
za kao patoloSka komponenta. Ateroskleroza je
dan je od glavnih uzroka infarkta miokarda, moZ
danog udara i perifernih vaskularnih bolesti, koji
 dine pribliZno polovinu svih smrtnih sludajeva u
 razvljenim zemljama. Ona ukljuduje orkestrira
ne procese endotelijalne disfunkcije, inflamacije,
 proliferacije VSMCs i reorganizaciju ekstracelu
larnog matriksa. Dediferencljacija i proliferacija
 VSMCs predstavljaju kljudne dogadaje u nastan
ku aterosklerotskih lezija, postangioplastidne re
stenoze i odbacivanja kalema pri bajpasu krvnih
 sudova.
 Trombin je moini modulator mnogih procesa kao
 Sto su regulisanje tonusa i propustljivosti krvnog
 suda, migracije i proliferacije VSMCs, privladenja
 monocita u aterosklerotske lezije i raznlh proin
flamatornih markera, a sve ovo,takode, doprinosi
 pro gresij i kardiovaskularnih oboljenja.
PB  - Beograd : Medicinski fakultet
T2  - Medicinska Istraživanja
T1  - Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMC) u aterosklerozi
VL  - 46
IS  - 2
SP  - 44
EP  - 53
UR  - https://hdl.handle.net/21.15107/rcub_cherry_6442
ER  - 

@article{
author = "Smiljanić, Katarina and Zafiroviç, Sonja and Obradovic, Milan and Gluvić, Zoran and Stokić, Edita and Putniković, Biljana and Isenović, Esma",
year = "2012",
abstract = "Glatke misićne ćelije krvnih sudova
 (VSMCs) su od vitalnog znaiaja, kako za struk
turu tako i za funkcionisanje i dinamiku krvnih
 sudova. Proliferacija i abnormalna akumulacija
 VSMCs su medu kljucnim dogadajima u nastan
ku raznih vaskularnih oboljenja, ukljudujuii ate
rosklerozu i hipertenziju. Kardiovaskularne bole
sti su vodeii uzrok smrtnosti ljudske populacije u
 dijoj osnovi u najveioj meri dominira aterosklero
za kao patoloSka komponenta. Ateroskleroza je
dan je od glavnih uzroka infarkta miokarda, moZ
danog udara i perifernih vaskularnih bolesti, koji
 dine pribliZno polovinu svih smrtnih sludajeva u
 razvljenim zemljama. Ona ukljuduje orkestrira
ne procese endotelijalne disfunkcije, inflamacije,
 proliferacije VSMCs i reorganizaciju ekstracelu
larnog matriksa. Dediferencljacija i proliferacija
 VSMCs predstavljaju kljudne dogadaje u nastan
ku aterosklerotskih lezija, postangioplastidne re
stenoze i odbacivanja kalema pri bajpasu krvnih
 sudova.
 Trombin je moini modulator mnogih procesa kao
 Sto su regulisanje tonusa i propustljivosti krvnog
 suda, migracije i proliferacije VSMCs, privladenja
 monocita u aterosklerotske lezije i raznlh proin
flamatornih markera, a sve ovo,takode, doprinosi
 pro gresij i kardiovaskularnih oboljenja.",
publisher = "Beograd : Medicinski fakultet",
journal = "Medicinska Istraživanja",
title = "Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMC) u aterosklerozi",
volume = "46",
number = "2",
pages = "44-53",
url = "https://hdl.handle.net/21.15107/rcub_cherry_6442"
}

Smiljanić, K., Zafiroviç, S., Obradovic, M., Gluvić, Z., Stokić, E., Putniković, B.,& Isenović, E.. (2012). Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMC) u aterosklerozi. in Medicinska Istraživanja
Beograd : Medicinski fakultet., 46(2), 44-53.
https://hdl.handle.net/21.15107/rcub_cherry_6442

Smiljanić K, Zafiroviç S, Obradovic M, Gluvić Z, Stokić E, Putniković B, Isenović E. Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMC) u aterosklerozi. in Medicinska Istraživanja. 2012;46(2):44-53.
https://hdl.handle.net/21.15107/rcub_cherry_6442 .

Smiljanić, Katarina, Zafiroviç, Sonja, Obradovic, Milan, Gluvić, Zoran, Stokić, Edita, Putniković, Biljana, Isenović, Esma, "Uloga trombina u proliferaciji glatkih mišićnih ćelija krvnih sudova (VSMC) u aterosklerozi" in Medicinska Istraživanja, 46, no. 2 (2012):44-53,
https://hdl.handle.net/21.15107/rcub_cherry_6442 .

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja
AU  - Zarić, Božidarka L.
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe
AU  - Mikhailidis, Dimitri
AU  - Rizzo, Manfredi
AU  - Isenović, Esma
PY  - 2012
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/3919
AB  - Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.
PB  - Nova Science Publishers Inc, New York
T2  - Ghrelin: Production, Action Mechanisms and Physiological Effects
T1  - Ghrelin, obesity and atherosclerosis
SP  - 111
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_cherry_3919
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja and Zarić, Božidarka L. and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe and Mikhailidis, Dimitri and Rizzo, Manfredi and Isenović, Esma",
year = "2012",
abstract = "Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.",
publisher = "Nova Science Publishers Inc, New York",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_cherry_3919"
}

Sudar, E., Soskić, S., Zarić, B. L., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ., Mikhailidis, D., Rizzo, M.,& Isenović, E.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects
Nova Science Publishers Inc, New York., 111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3919

Sudar E, Soskić S, Zarić BL, Rašić-Milutinović Z, Smiljanić K, Radak Đ, Mikhailidis D, Rizzo M, Isenović E. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3919 .

Sudar, Emina, Soskić, Sanja, Zarić, Božidarka L., Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe, Mikhailidis, Dimitri, Rizzo, Manfredi, Isenović, Esma, "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_cherry_3919 .

TY  - CHAP
AU  - Sudar, Emina
AU  - Soskić, Sanja
AU  - Zarić, Božidarka L.
AU  - Rašić-Milutinović, Zorica
AU  - Smiljanić, Katarina
AU  - Radak, Đorđe
AU  - Mikhailidis, Dimitri
AU  - Rizzo, Manfredi
AU  - Isenović, Esma
PY  - 2012
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/3920
AB  - Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.
PB  - Nova Science Publishers Inc, New York
T2  - Ghrelin: Production, Action Mechanisms and Physiological Effects
T1  - Ghrelin, obesity and atherosclerosis
SP  - 111
EP  - 126
UR  - https://hdl.handle.net/21.15107/rcub_cherry_3920
ER  - 

@inbook{
author = "Sudar, Emina and Soskić, Sanja and Zarić, Božidarka L. and Rašić-Milutinović, Zorica and Smiljanić, Katarina and Radak, Đorđe and Mikhailidis, Dimitri and Rizzo, Manfredi and Isenović, Esma",
year = "2012",
abstract = "Cardiovascular disease (CVD) is common cause of death in humans and its major underlying pathology is atherosclerosis. Atherosclerosis is a chronic inflammatory disease that predisposes to coronary artery disease (CAD), stroke and peripheral arterial disease, responsible for most of the cardiovascular morbidity and mortality. This inflammatory process, triggered by the presence of lipids in the vascular wall, and encompasses a complex interaction among inflammatory cells, vascular elements, and lipoproteins through the expression of several adhesion molecules and cytokines. Obesity is a risk factor for CVD but this association is not fully understood. Altered levels of obesity related peptides such as ghrelin may play an important role in this pathophysiology. Recent evidence indicates that ghrelin features several cardiovascular activities, including increased myocardial contractility, vasodilatation and protection from myocardial infarction. Recent data demonstrate that ghrelin can influence important key events in atherogenesis and thus they may play a role in atherosclerosis. In this review we present the latest data from recent animal and clinical studies which focus on a novel approach to ghrelin as a potential therapeutic agent in the treatment of a complex disease like atherosclerosis. Thus, ghrelin may become a new therapeutic target for the treatment of CVD. Further studies are necessary to investigate the potential mechanisms involved in the effects of ghrelin on the cardiovascular system.",
publisher = "Nova Science Publishers Inc, New York",
journal = "Ghrelin: Production, Action Mechanisms and Physiological Effects",
booktitle = "Ghrelin, obesity and atherosclerosis",
pages = "111-126",
url = "https://hdl.handle.net/21.15107/rcub_cherry_3920"
}

Sudar, E., Soskić, S., Zarić, B. L., Rašić-Milutinović, Z., Smiljanić, K., Radak, Đ., Mikhailidis, D., Rizzo, M.,& Isenović, E.. (2012). Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects
Nova Science Publishers Inc, New York., 111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3920

Sudar E, Soskić S, Zarić BL, Rašić-Milutinović Z, Smiljanić K, Radak Đ, Mikhailidis D, Rizzo M, Isenović E. Ghrelin, obesity and atherosclerosis. in Ghrelin: Production, Action Mechanisms and Physiological Effects. 2012;:111-126.
https://hdl.handle.net/21.15107/rcub_cherry_3920 .

Sudar, Emina, Soskić, Sanja, Zarić, Božidarka L., Rašić-Milutinović, Zorica, Smiljanić, Katarina, Radak, Đorđe, Mikhailidis, Dimitri, Rizzo, Manfredi, Isenović, Esma, "Ghrelin, obesity and atherosclerosis" in Ghrelin: Production, Action Mechanisms and Physiological Effects (2012):111-126,
https://hdl.handle.net/21.15107/rcub_cherry_3920 .

TY  - JOUR
AU  - Popović, Milan
AU  - Smiljanić, Katarina
AU  - Dobutović, Branislava
AU  - Syrovets, Tatiana
AU  - Simmet, Thomas
AU  - Isenovic, Esma R.
PY  - 2012
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/1220
AB  - Vascular endothelium is a key regulator of homeostasis. In physiological conditions it mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. However, endothelial dysfunction caused by physical injury of the vascular wall, for example during balloon angioplasty, acute or chronic inflammation, such as in atherothrombosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites. At the same time, the dysfunction promotes thrombin generation, fibrin deposition, and coagulation. The serine protease thrombin plays a pivotal role in the coagulation cascade. However, thrombin is not only the key effector of coagulation cascade; it also plays a significant role in inflammatory diseases. It shows an array of effects on endothelial cells, vascular smooth muscle cells, monocytes, and platelets, all of which participate in the vascular pathophysiology such as atherothrombosis. Therefore, thrombin can be considered as an important modulatory molecule of vascular homeostasis. This review summarizes the existing evidence on the role of thrombin in vascular inflammation.
PB  - Springer, Dordrecht
T2  - Molecular and Cellular Biochemistry
T1  - Thrombin and vascular inflammation
VL  - 359
IS  - 1-2
SP  - 301
EP  - 313
DO  - 10.1007/s11010-011-1024-x
ER  - 

@article{
author = "Popović, Milan and Smiljanić, Katarina and Dobutović, Branislava and Syrovets, Tatiana and Simmet, Thomas and Isenovic, Esma R.",
year = "2012",
abstract = "Vascular endothelium is a key regulator of homeostasis. In physiological conditions it mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. However, endothelial dysfunction caused by physical injury of the vascular wall, for example during balloon angioplasty, acute or chronic inflammation, such as in atherothrombosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites. At the same time, the dysfunction promotes thrombin generation, fibrin deposition, and coagulation. The serine protease thrombin plays a pivotal role in the coagulation cascade. However, thrombin is not only the key effector of coagulation cascade; it also plays a significant role in inflammatory diseases. It shows an array of effects on endothelial cells, vascular smooth muscle cells, monocytes, and platelets, all of which participate in the vascular pathophysiology such as atherothrombosis. Therefore, thrombin can be considered as an important modulatory molecule of vascular homeostasis. This review summarizes the existing evidence on the role of thrombin in vascular inflammation.",
publisher = "Springer, Dordrecht",
journal = "Molecular and Cellular Biochemistry",
title = "Thrombin and vascular inflammation",
volume = "359",
number = "1-2",
pages = "301-313",
doi = "10.1007/s11010-011-1024-x"
}

Popović, M., Smiljanić, K., Dobutović, B., Syrovets, T., Simmet, T.,& Isenovic, E. R.. (2012). Thrombin and vascular inflammation. in Molecular and Cellular Biochemistry
Springer, Dordrecht., 359(1-2), 301-313.
https://doi.org/10.1007/s11010-011-1024-x

Popović M, Smiljanić K, Dobutović B, Syrovets T, Simmet T, Isenovic ER. Thrombin and vascular inflammation. in Molecular and Cellular Biochemistry. 2012;359(1-2):301-313.
doi:10.1007/s11010-011-1024-x .

Popović, Milan, Smiljanić, Katarina, Dobutović, Branislava, Syrovets, Tatiana, Simmet, Thomas, Isenovic, Esma R., "Thrombin and vascular inflammation" in Molecular and Cellular Biochemistry, 359, no. 1-2 (2012):301-313,
https://doi.org/10.1007/s11010-011-1024-x . .

TY  - JOUR
AU  - Popović, Milan
AU  - Smiljanić, Katarina
AU  - Dobutović, Branislava
AU  - Syrovets, Tatiana
AU  - Simmet, Thomas
AU  - Isenovic, Esma R.
PY  - 2012
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/1243
AB  - Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to intima-media thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor kappa B, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the intima of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.
PB  - Springer, Dordrecht
T2  - Journal of Thrombosis and Thrombolysis
T1  - Human cytomegalovirus infection and atherothrombosis
VL  - 33
IS  - 2
SP  - 160
EP  - 172
DO  - 10.1007/s11239-011-0662-x
ER  - 

@article{
author = "Popović, Milan and Smiljanić, Katarina and Dobutović, Branislava and Syrovets, Tatiana and Simmet, Thomas and Isenovic, Esma R.",
year = "2012",
abstract = "Vascular endothelium, as a key regulator of hemostasis, mediates vascular dilatation, prevents platelet adhesion, and inhibits thrombin generation. Endothelial dysfunction caused by acute or chronic inflammation, such as in atherosclerosis, creates a proinflammatory environment which supports leukocyte transmigration toward inflammatory sites, and at the same time promotes coagulation, thrombin generation, and fibrin deposition in an attempt to close the wound. Life-long persistent infection with human cytomegalovirus (HCMV) has been associated with atherosclerosis. In vivo studies have revealed that HCMV infection of the vessel wall affects various cells including monocytes/macrophages, smooth muscle cells (SMCs) and endothelial cells (ECs). HCMV-infected SMCs within vascular lesions display enhanced proliferation and impaired apoptosis, which contribute to intima-media thickening, plaque formation and restenosis. Monocytes play a central role in the process of viral dissemination, whereas ECs may represent a viral reservoir, maintaining persistent infection in HCMV-infected atherosclerotic patients following the primary infection. Persistent infection leads to dysfunction of ECs and activates proinflammatory signaling involving nuclear factor kappa B, specificity protein 1, and phosphatidylinositol 3-kinase, as well as expression of platelet-derived growth factor receptor. Activation of these pathways promotes enhanced proliferation and migration of monocytes and SMCs into the intima of the vascular wall as well as lipid accumulation and expansion of the atherosclerotic lesion. Moreover, HCMV infection induces enhanced expression of endothelial adhesion molecules and modifies the proteolytic balance in monocytes and macrophages. As a consequence, infected endothelium recruits naive monocytes from the blood stream, and the concomitant interaction between infected ECs and monocytes enables virus transfer to migrating monocytes. Endothelial damage promotes thrombin generation linking inflammation and coagulation. HCMV, in turn, enhances the thrombin generation. The virus carries on its surface the molecular machinery necessary to initiate thrombin generation, and in addition, may interact with the prothrombinase protein complex thereby facilitating thrombin generation. Thus, infection of endothelium may significantly increase the production of thrombin. This might not only contribute to thrombosis in patients with atherosclerosis, but might also induce thrombin-dependent proinflammatory cell activation. This review summarizes the existing evidence on the role of HCMV in vascular inflammation.",
publisher = "Springer, Dordrecht",
journal = "Journal of Thrombosis and Thrombolysis",
title = "Human cytomegalovirus infection and atherothrombosis",
volume = "33",
number = "2",
pages = "160-172",
doi = "10.1007/s11239-011-0662-x"
}

Popović, M., Smiljanić, K., Dobutović, B., Syrovets, T., Simmet, T.,& Isenovic, E. R.. (2012). Human cytomegalovirus infection and atherothrombosis. in Journal of Thrombosis and Thrombolysis
Springer, Dordrecht., 33(2), 160-172.
https://doi.org/10.1007/s11239-011-0662-x

Popović M, Smiljanić K, Dobutović B, Syrovets T, Simmet T, Isenovic ER. Human cytomegalovirus infection and atherothrombosis. in Journal of Thrombosis and Thrombolysis. 2012;33(2):160-172.
doi:10.1007/s11239-011-0662-x .

Popović, Milan, Smiljanić, Katarina, Dobutović, Branislava, Syrovets, Tatiana, Simmet, Thomas, Isenovic, Esma R., "Human cytomegalovirus infection and atherothrombosis" in Journal of Thrombosis and Thrombolysis, 33, no. 2 (2012):160-172,
https://doi.org/10.1007/s11239-011-0662-x . .

TY  - JOUR
AU  - Smiljanić, Katarina
AU  - Dobutovic, B.
AU  - Obradović, Milan
AU  - Nikolić, D.
AU  - Marche, P.
AU  - Isenovic, E. R.
PY  - 2011
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/1195
AB  - Cardiovascular disease is the largest single cause of mortality and its major underlying pathology is atherosclerosis. The proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of the various vascular diseases, including atherosclerosis and hypertension. Thrombin (Thr) is involved in the abnormal proliferation of VSMCs associated with atherosclerosis and hypertension. ADAMs (A Disintegrin And Metalloproteinase) are transmembrane metalloproteinases, belonging to the adamalysins group, that are distinct from matrix metalloproteinases (MMPs) in a way as they have an extracellular disintegrin domain and cytoplasmic domain that can associate with intracellular proteins. There is limited knowledge about the presence of ADAM metalloproteinase activity in Thr-induced VSMCs proliferation. Therefore, this review examines recent findings in signaling mechanisms employed by Thr in modulating the regulation of proliferation of VSMCs with particular emphasis on involvement of ADAM 12 which has been identified as an important mediator of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of Thr in vascular biology and vascular diseases.
PB  - Bentham Science Publ Ltd, Sharjah
T2  - Current Medicinal Chemistry
T1  - Involvement of the ADAM 12 in Thrombin-Induced Rat's VSMCs Proliferation
VL  - 18
IS  - 22
SP  - 3382
EP  - 3386
DO  - 10.2174/092986711796504709
ER  - 

@article{
author = "Smiljanić, Katarina and Dobutovic, B. and Obradović, Milan and Nikolić, D. and Marche, P. and Isenovic, E. R.",
year = "2011",
abstract = "Cardiovascular disease is the largest single cause of mortality and its major underlying pathology is atherosclerosis. The proliferation of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of the various vascular diseases, including atherosclerosis and hypertension. Thrombin (Thr) is involved in the abnormal proliferation of VSMCs associated with atherosclerosis and hypertension. ADAMs (A Disintegrin And Metalloproteinase) are transmembrane metalloproteinases, belonging to the adamalysins group, that are distinct from matrix metalloproteinases (MMPs) in a way as they have an extracellular disintegrin domain and cytoplasmic domain that can associate with intracellular proteins. There is limited knowledge about the presence of ADAM metalloproteinase activity in Thr-induced VSMCs proliferation. Therefore, this review examines recent findings in signaling mechanisms employed by Thr in modulating the regulation of proliferation of VSMCs with particular emphasis on involvement of ADAM 12 which has been identified as an important mediator of VSMCs hypertrophy and vascular diseases. These findings are critical for understanding the role of Thr in vascular biology and vascular diseases.",
publisher = "Bentham Science Publ Ltd, Sharjah",
journal = "Current Medicinal Chemistry",
title = "Involvement of the ADAM 12 in Thrombin-Induced Rat's VSMCs Proliferation",
volume = "18",
number = "22",
pages = "3382-3386",
doi = "10.2174/092986711796504709"
}

Smiljanić, K., Dobutovic, B., Obradović, M., Nikolić, D., Marche, P.,& Isenovic, E. R.. (2011). Involvement of the ADAM 12 in Thrombin-Induced Rat's VSMCs Proliferation. in Current Medicinal Chemistry
Bentham Science Publ Ltd, Sharjah., 18(22), 3382-3386.
https://doi.org/10.2174/092986711796504709

Smiljanić K, Dobutovic B, Obradović M, Nikolić D, Marche P, Isenovic ER. Involvement of the ADAM 12 in Thrombin-Induced Rat's VSMCs Proliferation. in Current Medicinal Chemistry. 2011;18(22):3382-3386.
doi:10.2174/092986711796504709 .

Smiljanić, Katarina, Dobutovic, B., Obradović, Milan, Nikolić, D., Marche, P., Isenovic, E. R., "Involvement of the ADAM 12 in Thrombin-Induced Rat's VSMCs Proliferation" in Current Medicinal Chemistry, 18, no. 22 (2011):3382-3386,
https://doi.org/10.2174/092986711796504709 . .

TY  - JOUR
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskić, Sanja
AU  - Dungen, Hans-Dirk
AU  - Isenović, Esma
PY  - 2011
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/3918
AB  - Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a free radical which reacts with various molecules to cause multiple biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are exquisitely regulated and extend to almost every cell type and function within the circulation. While the molecule mediates many physiological functions, an excessive presence of NO is toxic to cells. The enzyme NOS, constitutively or inductively, catalyses the production of NO in several biological systems. NO is derived not only from NOS isoforms but also from NOS-independent sources. In mammals, to date, three distinct NOS isoforms have been identified: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). The molecular structure, enzymology and pharmacology of these enzymes have been well defined, and reveal critical roles for the NOS system in a variety of important physiological processes. This review focuses on recent advances in the understanding of the interactions between NOS enzymes and pathophysiology of cardiovascular diseases (CVD) and the role of NO agonists as potential therapeutic agents in treatment of CVD.
PB  - Bentham Open
T2  - The Open Nitric Oxide Journal
T1  - Nitric Oxide and its Role in Cardiovascular Diseases
VL  - 3
IS  - 1
SP  - 65
EP  - 71
DO  - 10.2174/1875042701103010065
ER  - 

@article{
author = "Dobutović, Branislava and Smiljanić, Katarina and Soskić, Sanja and Dungen, Hans-Dirk and Isenović, Esma",
year = "2011",
abstract = "Nitric oxide synthases (NOS) are the enzymes responsible for nitric oxide (NO) generation. NO is a free radical which reacts with various molecules to cause multiple biological effects. It is clear that the generation and actions of NO under physiological and pathophysiological conditions are exquisitely regulated and extend to almost every cell type and function within the circulation. While the molecule mediates many physiological functions, an excessive presence of NO is toxic to cells. The enzyme NOS, constitutively or inductively, catalyses the production of NO in several biological systems. NO is derived not only from NOS isoforms but also from NOS-independent sources. In mammals, to date, three distinct NOS isoforms have been identified: neuronal NOS (nNOS), inducible NOS (iNOS), and endothelial NOS (eNOS). The molecular structure, enzymology and pharmacology of these enzymes have been well defined, and reveal critical roles for the NOS system in a variety of important physiological processes. This review focuses on recent advances in the understanding of the interactions between NOS enzymes and pathophysiology of cardiovascular diseases (CVD) and the role of NO agonists as potential therapeutic agents in treatment of CVD.",
publisher = "Bentham Open",
journal = "The Open Nitric Oxide Journal",
title = "Nitric Oxide and its Role in Cardiovascular Diseases",
volume = "3",
number = "1",
pages = "65-71",
doi = "10.2174/1875042701103010065"
}

Dobutović, B., Smiljanić, K., Soskić, S., Dungen, H.,& Isenović, E.. (2011). Nitric Oxide and its Role in Cardiovascular Diseases. in The Open Nitric Oxide Journal
Bentham Open., 3(1), 65-71.
https://doi.org/10.2174/1875042701103010065

Dobutović B, Smiljanić K, Soskić S, Dungen H, Isenović E. Nitric Oxide and its Role in Cardiovascular Diseases. in The Open Nitric Oxide Journal. 2011;3(1):65-71.
doi:10.2174/1875042701103010065 .

Dobutović, Branislava, Smiljanić, Katarina, Soskić, Sanja, Dungen, Hans-Dirk, Isenović, Esma, "Nitric Oxide and its Role in Cardiovascular Diseases" in The Open Nitric Oxide Journal, 3, no. 1 (2011):65-71,
https://doi.org/10.2174/1875042701103010065 . .

TY  - JOUR
AU  - Haidara, Mohamed
AU  - Mikhailidis, Dimitri P.
AU  - Yassin, Hanaa Z.
AU  - Dobutović, Branislava
AU  - Smiljanić, Katarina
AU  - Soskic, Sanja
AU  - Mousa, Shaker A.
AU  - Rizzo, Manfredi
AU  - Isenovic, Esma R.
PY  - 2011
UR  - https://cherry.chem.bg.ac.rs/handle/123456789/1242
AB  - The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.
PB  - Bentham Science Publ Ltd, Sharjah
T2  - Current Pharmaceutical Design
T1  - Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome
VL  - 17
IS  - 33
SP  - 3699
EP  - 3712
DO  - 10.2174/138161211798220882
ER  - 

@article{
author = "Haidara, Mohamed and Mikhailidis, Dimitri P. and Yassin, Hanaa Z. and Dobutović, Branislava and Smiljanić, Katarina and Soskic, Sanja and Mousa, Shaker A. and Rizzo, Manfredi and Isenovic, Esma R.",
year = "2011",
abstract = "The metabolic syndrome (MetS) is common, and its associated risk burdens of diabetes and cardiovascular disease (CVD) are a major public health problem. The hypothesis that main constituent parameters of the MetS share common pathophysiologic mechanisms provides a conceptual framework for the future research. Exercise and weight loss can prevent insulin resistance and reduce the risk of diseases associated with the MetS. Interrupting intracellular and extracellular reactive oxygen species (ROS) overproduction could also contribute to normalizing the activation of metabolic pathways leading to the onset of diabetes, endothelial dysfunction, and cardiovascular (CV) complications. On the other hand, it is difficult to counteract the development of CV complications by using conventional antioxidants. Indeed, interest has focused on strategies that enhance the removal of ROS using either antioxidants or drugs that enhance endogenous antioxidant defense. Although these strategies have been effective in laboratory experiments, several clinical trials have shown that they do not reduce CV events, and in some cases antioxidants have actually worsened the outcome. More research is needed in this field.",
publisher = "Bentham Science Publ Ltd, Sharjah",
journal = "Current Pharmaceutical Design",
title = "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome",
volume = "17",
number = "33",
pages = "3699-3712",
doi = "10.2174/138161211798220882"
}

Haidara, M., Mikhailidis, D. P., Yassin, H. Z., Dobutović, B., Smiljanić, K., Soskic, S., Mousa, S. A., Rizzo, M.,& Isenovic, E. R.. (2011). Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design
Bentham Science Publ Ltd, Sharjah., 17(33), 3699-3712.
https://doi.org/10.2174/138161211798220882

Haidara M, Mikhailidis DP, Yassin HZ, Dobutović B, Smiljanić K, Soskic S, Mousa SA, Rizzo M, Isenovic ER. Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome. in Current Pharmaceutical Design. 2011;17(33):3699-3712.
doi:10.2174/138161211798220882 .

Haidara, Mohamed, Mikhailidis, Dimitri P., Yassin, Hanaa Z., Dobutović, Branislava, Smiljanić, Katarina, Soskic, Sanja, Mousa, Shaker A., Rizzo, Manfredi, Isenovic, Esma R., "Evaluation of the Possible Contribution of Antioxidants Administration in Metabolic Syndrome" in Current Pharmaceutical Design, 17, no. 33 (2011):3699-3712,
https://doi.org/10.2174/138161211798220882 . .