Open AccessCalcium Signal Pathway is Involved in Prostaglandin E2 Induced Cardiac Fibrosis in Cardiac Fibroblasts
Author(s) -
Yunzi Ma,
Zhongbao Yue,
Boyu Zhang,
Min Yang,
Haiyan Lao,
WenTer Lai,
Yingtong Zeng,
ShaoRui Chen,
Peiqing Liu
Publication year - 2018
Publication title -
journal of pharmacy and pharmaceutical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.497
H-Index - 78
ISSN - 1482-1826
DOI - 10.18433/jpps29322
Subject(s) - ctgf , arachidonic acid , prostaglandin e2 receptor , cardiac fibrosis , downregulation and upregulation , fibrosis , fibronectin , prostaglandin e2 , chemistry , calcium in biology , western blot , signal transduction , immunostaining , connective tissue , microbiology and biotechnology , endocrinology , prostaglandin , medicine , receptor , growth factor , biology , agonist , biochemistry , pathology , cell , immunohistochemistry , gene , enzyme
Prostaglandin E2 (PGE2), one of the arachidonic acid metabolites synthetized from arachidonic acid through cyclooxygenase (COX) catalysis, demonstrates multiple physiological and pathological actions through different subtypes of EP receptors. PURPOSE: The present study was designed to explore the effects of PGE2 on cardiac fibrosis and the involved mechanism. METHODS: We used western blot analysis, real-time quantitative PCR and immunostaining etc. to testify the mechanism. RESULTS: Our data showed that in cultured adult rat cardiac fibroblasts (CFs), PGE2 effectively promoted the expression of α-smooth muscle actin (α-SMA), connective tissue growth factor (CTGF)fibronectin (FN), Collagen I and induced [Ca2+]i increase. Besides, calcium increase evoked by PGE2 is mediated by virtue of EP1 activation. Instead of EP3 or EP4, inhibition of EP1 attenuated PGE2-stimulated upregulation of α-SMACTGF, FN, collagen I and [Ca2+]i, as well as the nuclear factor of activated T cell cytoplasmic 4 protein (NFATc4) translocation. CONCLUSIONS: PGE2 may promote cardiac fibrosis via EP1 receptor and calcium signal pathway.