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Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2
dc.creator | Smiljanić, Katarina | |
dc.creator | Obradović, Milan M. | |
dc.creator | Jovanović, Aleksandra | |
dc.creator | Đorđević, Jelena D. | |
dc.creator | Dobutović, Branislava | |
dc.creator | Jevremovic, Danimir | |
dc.creator | Marche, Pierre | |
dc.creator | Isenović, Esma R. | |
dc.date.accessioned | 2018-03-01T15:29:02Z | |
dc.date.available | 2018-03-01T15:29:02Z | |
dc.date.issued | 2014 | |
dc.identifier.issn | 0300-8177 | |
dc.identifier.issn | 1573-4919 | |
dc.identifier.uri | https://vinar.vin.bg.ac.rs/handle/123456789/134 | |
dc.description.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. | en |
dc.relation | info:eu-repo/grantAgreement/MESTD/Basic Research (BR or ON)/173033/RS// | |
dc.relation | CNRS, University Pierre and Marie Curie, Republic of France, Ministry of Foreign Affairs, [337-00-359/2005-01/16] | |
dc.rights | restrictedAccess | en |
dc.source | Molecular and Cellular Biochemistry | en |
dc.subject | Thrombin signaling cascade | en |
dc.subject | Pathological VSMC proliferation | en |
dc.subject | MMP-2 | en |
dc.subject | EGFR transactivation | en |
dc.subject | Atherosclerosis | en |
dc.subject | Matrix metalloproteinase | en |
dc.subject | Heparin-binding epidermal growth factor like | en |
dc.title | Thrombin stimulates VSMC proliferation through an EGFR-dependent pathway: involvement of MMP-2 | en |
dc.type | article | en |
dcterms.abstract | Исеновић Есма; Смиљанић Катарина; Јовановић Aлександра; Обрадовић Милан; Дјордјевиц, Јелена; Марцхе, Пиерре; Јевремовиц, Данимир; Добутовиц, Бранислава; | |
dc.citation.volume | 396 | |
dc.citation.issue | 1-2 | |
dc.citation.spage | 147 | |
dc.citation.epage | 160 | |
dc.identifier.wos | 000342437900016 | |
dc.identifier.doi | 10.1007/s11010-014-2151-y | |
dc.citation.rank | M23 | |
dc.identifier.pmid | 25047892 | |
dc.type.version | publishedVersion | |
dc.identifier.scopus | 2-s2.0-84907593049 |
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