Hong-yan Dai1, Zhi-ming Ge, Yong-hong Li. 1. Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Public Health, Shandong University, Jinan 250012, China.
Abstract
OBJECTIVE: To study the effect of urotensin II ( U II ) on the proliferative potential of adventitial fibroblasts (AFs) from spontaneously hypertensive rat (SHR) and to determine whether extracellular signal-regulated kinase 1/2 (ERK1/2) pathway is involved in this progress. METHODS: 3H-thymidine incorporation test was used to estimate the U II -induced proliferative potential of AFs from SHR and the influence of Urantide (U II receptor antagonist) and PD98059 (ERK1/2 inhibitor). Western blotting was used to test the U II -induced ERK1/2 phosphorylation as well as the effect of Urantide and PD98059 on U II -induced ERKl/2 phosphorylation. RESULTS: U 11 increased the proliferative potential of AFs from SHR in a dose-dependent way. Urantide and PD98059 wholly or partly inhibited U II -induced proliferation of SHR-AFs. In SHR-AFs, U II induced the phosphorylation of ERK1/2 in a time-dependent way, which was completely inhibited by Urantide and PD98059. CONCLUSION: U II can increase the proliferative potential of AFs from SHR and ERK1/2 pathway is partly involved in this progress.
OBJECTIVE: To study the effect of urotensin II ( U II ) on the proliferative potential of adventitial fibroblasts (AFs) from spontaneously hypertensiverat (SHR) and to determine whether extracellular signal-regulated kinase 1/2 (ERK1/2) pathway is involved in this progress. METHODS:3H-thymidine incorporation test was used to estimate the U II -induced proliferative potential of AFs from SHR and the influence of Urantide (U II receptor antagonist) and PD98059 (ERK1/2 inhibitor). Western blotting was used to test the U II -induced ERK1/2 phosphorylation as well as the effect of Urantide and PD98059 on U II -induced ERKl/2 phosphorylation. RESULTS: U 11 increased the proliferative potential of AFs from SHR in a dose-dependent way. Urantide and PD98059 wholly or partly inhibited U II -induced proliferation of SHR-AFs. In SHR-AFs, U II induced the phosphorylation of ERK1/2 in a time-dependent way, which was completely inhibited by Urantide and PD98059. CONCLUSION:U II can increase the proliferative potential of AFs from SHR and ERK1/2 pathway is partly involved in this progress.