Effect of β3-adrenoceptor on cardiac fibrosis in rat cardiac fibroblast cells and its potential mechanism


Autoria(s): Zhang, Yuan; Zhang, Hui; Ma, Yitong; Yang, Yining; Ma, Miaomiao; Zhu, Xiaoli; Wang, Li
Cobertura

Origin of publication: Nigeria

Data(s)

01/06/2016

Resumo

Purpose: To investigate the effect of β3-adrenoceptors (β3-AR) up-regulation on fibrosis in cardiac fibroblast cells in rats and its potential mechanism. Methods: Cardiac fibroblast cells (CFB) were isolated and identified from rats’ hearts. The β3-ARupregulated cardiac fibroblast cells were constructed by lentiviral transfection technology. Thereafter, Ang II was used to induce fibrosis in cardiac fibroblast cells, and subsequently, Western blot assay was performed to investigate fibrosis related marker proteins (TGF-β, Smad-2, p-Smad-2, Col-I and Col-III) in cardiac fibroblast cells. Results: β3-AR up-regulated cardiac fibroblast cells were successfully constructed. Furthermore, the results show that up-regulation of β3-AR increased the expressions of TGF-β, p-Smad-2, Col-I and Col- III proteins in Ang II treated cardiac fibroblast cells. Conclusion: The results suggest that up-regulation of β3-AR aggravates fibrosis of cardiac fibroblast cells. In other words, inhibition of β3-AR expressions in cardiac tissues would be beneficial for treating cardiac fibrosis and its related cardiac diseases.

Formato

html

Identificador

http://www.bioline.org.br/abstract?id=pr16095

Idioma(s)

en

Publicador

Pharmacotherapy Group, Faculty of Pharmacy, University of Benin, Benin City, Nigeria

Relação

http://www.tjpr.org; http://www.bioline.org.br/pr

Direitos

Copyright 2016 - Tropical Journal of Pharmaceutical Research

Fonte

Tropical Journal of Pharmaceutical Research (ISSN: 1596-5996) Vol 15 Num 4

Palavras-Chave #Cardiac fibrosis; TGF/Smads; Cardiac fibroblast cells; β3-AR; Col-I/III
Tipo

AA