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Urotensin‐2 promotes collagen synthesis via ERK1/2‐dependent and ERK1/2‐independent TGF‐β1 in neonatal cardiac fibroblasts
Author(s) -
Dai HongYan,
He Tao,
Li XiaoLu,
Xu WenLiang,
Ge ZhiMing
Publication year - 2011
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20090104
Subject(s) - cardiac fibrosis , transforming growth factor , microbiology and biotechnology , kinase , signal transduction , chemistry , urotensin ii , extracellular , fibroblast , fibrosis , endocrinology , medicine , biology , biochemistry , receptor , in vitro
U2 (urotensin‐2) is the most potent vasoconstrictor in mammals which is involved in cardiac remodelling, including cardiac hypertrophy and cardiac fibrosis. Although the cellular mechanisms of the U2‐induced vasoconstriction have been extensively studied, the signalling pathways involved in U2‐induced TGF‐β1 (transforming growth factor‐β1) expression and collagen synthesis remain unclear. In this study, we show that U2 promoted collagen synthesis and ERK1/2 (extracellular signal‐regulated kinase 1/2) activation in neonatal cardiac fibroblasts. The U2‐induced collagen synthesis and TGF‐β1 production were significantly but not completely inhibited by blocking ERK1/2. Both ERK1/2 inhibitor and TGF‐β1 antibody could separately inhibit U2‐induced collagen synthesis, and the synergistic inhibition effect was observed by blocking ERK1/2 and TGF‐β1 simultaneously. These data suggest that U2 promotes collagen synthesis via ERK1/2‐dependent and independent TGF‐β1 pathway in neonatal cardiac fibroblasts.