G protein-coupled estrogen receptor1 (GPER1) may mediate Rho-kinase (ROCK-2) up-regulation in coronary endothelial cells
dc.contributor.author | Kurt A.H. | |
dc.contributor.author | Tiftik R.N. | |
dc.contributor.author | Un I. | |
dc.contributor.author | Ulker S. | |
dc.contributor.author | Buyukafsar K. | |
dc.date.accessioned | 2019-10-26T21:36:20Z | |
dc.date.available | 2019-10-26T21:36:20Z | |
dc.date.issued | 2013 | |
dc.department | Ege Üniversitesi | en_US |
dc.description.abstract | objective. Efect of estrogenic compounds and 17ß-estradiol (E2), which induces endothelial cell motility, was investigated on ROCK-2 expression in rat coronary vascular endothelial cells (CVEC). Methods. Te CVEC were isolated from the heart of Wistar rats by collagenase (0.04%) and incubated with E2 (1-100 nM), estrogen receptor ? (ER?) agonist: propyl pyrazole triol (PPT, 10 nM); ERß agonists: (2,3-bis(4-hydroxyphenyl)-propionitrile, DPN, 10 nM) and E2-conjugate with bovine serum albumin (E2-BSA, 1 nM); and GPER1 agonist: G1 (100 nM). Furthermore, the efect of combination of E2 with estrogen receptors (ERs) antagonist and GPER1 agonist, ICI-182780 (10 µM), physiological estrogen antagonists: progesterone (P4, 10-100 nM) and testosterone (T, 10-100 nM); transcription inhibitor: actinomycin-D (1 µg/ml); GPER1 antagonist: G-15 (100 nM), superoxide dismutase, (SOD, 500 U/ml); Gi/o protein inhibitor: pertussis toxin (PTX, 100 µg/ml); and epidermal growth factor receptor (EGFR) blocker: AG-1478 (10 µM) was tested. After 24h incubation, ROCK-2 and GPER1 protein expressions were detected in the CVEC by Western-blotting. results. E2, ICI-182780, and G1 but not E2-BSA signifcantly up-regulated ROCK-2 expression, which was suppressed by actinomycin-D, PTX, AG-1478, and G-15. However, PPT and DPN had no efects on the ROCK-2 expression. ICI-182780, P4, T or SOD did not antagonize the E2 action. GPER1 expression was demonstrated in the CVEC. Conclusions. Estrogens could up-regulate ROCK-2 in the rat CVEC through GPER1 and EGFR transactivation. | en_US |
dc.identifier.doi | 10.4149/endo_2013_02_75 | en_US |
dc.identifier.endpage | 84 | en_US |
dc.identifier.issn | 1210-0668 | |
dc.identifier.issue | 2 | en_US |
dc.identifier.pmid | 23641788 | en_US |
dc.identifier.scopusquality | Q3 | en_US |
dc.identifier.startpage | 75 | en_US |
dc.identifier.uri | https://doi.org/10.4149/endo_2013_02_75 | |
dc.identifier.uri | https://hdl.handle.net/11454/17998 | |
dc.identifier.volume | 47 | en_US |
dc.indekslendigikaynak | Scopus | en_US |
dc.indekslendigikaynak | PubMed | en_US |
dc.language.iso | en | en_US |
dc.relation.ispartof | Endocrine Regulations | en_US |
dc.relation.publicationcategory | Makale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanı | en_US |
dc.rights | info:eu-repo/semantics/closedAccess | en_US |
dc.subject | 17ß-estradiol | en_US |
dc.subject | Endothelium | en_US |
dc.subject | GPER1 | en_US |
dc.subject | ICI-182780 | en_US |
dc.subject | Rho-kinase | en_US |
dc.title | G protein-coupled estrogen receptor1 (GPER1) may mediate Rho-kinase (ROCK-2) up-regulation in coronary endothelial cells | en_US |
dc.type | Article | en_US |