TITLE:
Antagonism of Angiotensin II AT1 Receptor and Silencing of CD44 Gene Expression Inhibit Cardiac Fibroblast Activation via Modulating TGF-β1/Smad Signaling Pathway
AUTHORS:
Feng Bai, Guangzhao Yang, Joshua Robert Eskew, Ningping Wang, Himangshu Bose, Zhiqing Zhao
KEYWORDS:
Angiotensin II AT1 Receptor, CD44, Collagen, Fibroblasts, Telmisartan
JOURNAL NAME:
Advances in Bioscience and Biotechnology,
Vol.11 No.4,
April
22,
2020
ABSTRACT: Angiotensin II (Ang II) is known to elicit cardiac
fibrosis by activating the AT1 receptor and CD44 expression in the in vivo model. However, the cellular/molecular
mechanisms underlying cardiac fibrosis are still not well understood. This
study examines the roles of the AT1 receptor and CD44 gene expression in
collagen synthesis through Ang II stimulated cardiac fibroblasts. Fibroblasts
were isolated from the neonatal rat hearts; the activation of fibroblasts was evaluated using
the assays of cell viability and migration, and silencing of CD44 gene
expression was conducted with small interfering RNA
(siRNA). Results showed that Ang II significantly increases the cell
proliferation and migration in a dose-dependent manner. Upon
activation, the protein levels of TGF-β1,
Smad2, Smad4 and collagen I were significantly increased (all p by the AT1 receptor
blocker, telmisartan (all p β1
as demonstrated by Pearson correlation analysis (r = 0.955, p