In:
Journal of Pharmacy & Pharmaceutical Sciences, Frontiers Media SA, Vol. 21 ( 2018-08-07), p. 326-339
Kurzfassung:
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-SMA，CTGF, 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.
Materialart:
Online-Ressource
ISSN:
1482-1826
,
1482-1826
Sprache:
Unbekannt
Verlag:
Frontiers Media SA
Publikationsdatum:
2018
ZDB Id:
1422972-9
SSG:
15,3
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