Article citationsMore>>

Khalil, H., Kanisicak, O., Prasad, V., Correll, RN., Fu, X., Schips, T., Vagnozzi, R.J., Liu, R., Huynh, T., Lee, S.J., Karch, J. and Molkentin, J.D. (2017) Fibroblast-Specific TGF-β-Smad2/3 Signaling Underlies Cardiacfibrosis. Journal of Clinical Investigation, 127, 3770-3783.
https://doi.org/10.1172/JCI94753

has been cited by the following article:

• 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