Effect of urotensin II on proliferative potential and phosphorylation of extracellular signal-regulated kinase 1/2 of adventitial fibroblasts from spontaneously hypertensive rat.
- Author:
Hong-yan DAI
1
;
Zhi-ming GE
;
Yong-hong LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Cell Proliferation; drug effects; Cells, Cultured; Fibroblasts; drug effects; enzymology; Flavonoids; pharmacology; Male; Mitogen-Activated Protein Kinase 3; drug effects; metabolism; Peptide Fragments; pharmacology; Phosphorylation; drug effects; Rats; Rats, Inbred SHR; Urotensins; pharmacology
- From: Acta Academiae Medicinae Sinicae 2006;28(6):776-780
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo 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.
METHODS3H-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.
RESULTSU 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.
CONCLUSIONU II can increase the proliferative potential of AFs from SHR and ERK1/2 pathway is partly involved in this progress.
