Abstract
To observe the effect of β3 adrenergic receptor (β3-AR) on fibrosis in cardiac fibroblasts(CFBs) and explore the related mechanisms. Neonatal CFBs were divided into negative control group (N-CFC): CFBs without any intervention; group treated with β3 adrenergic receptor agonist (AngⅡ-CFC-β3-AR BRL): CFBs treated with 10(-6) mol/L angiotensin Ⅱ(AngⅡ), 1 hour later treated with 10(-5) mol/L β3 adrenergic receptor agonist (β3-AR BRL37344); group treated with β3 adrenergic receptor antagonist (AngⅡ-CFC-β3-AR SR): CFBs treated with 10(-6) mol/L AngⅡ, 1 hour later treated with 10(-5) mol/L β3 adrenergic receptor antagonist (β3-AR SR59230A); and positive control group (AngⅡ-CFC): CFBs treated with 10(-6) mol/L AngⅡonly. Proliferation of CFBs was detected by the method of WST-1. Protein expression of β3-AR, transforming growth factor β1 receptor (TGF-β1-R), transforming growth factor β1(TGF-β1), Smad-2, phospho-Smad-2 (p-Smad-2), collagen-Ⅰ (COL-Ⅰ) and collagen-Ⅲ(COL-Ⅲ) was determined by Western blot assay. (1) The proliferation of CFBs was the highest in AngⅡ-CFC-β3-AR BRL, followed by AngⅡ-CFC-β3-AR SR and AngⅡ-CFC group (all P<0.05 vs. N-CFC group). (2) The protein expression level of β3-AR, TGF-β1-R, TGF-β1 and p-Smad-2 was in the same order as proliferation of CFBs. (3) The expression level of COL-Ⅰ and COL-Ⅲ protein was also in the same order as proliferation of CFBs. Activation of β3-AR may promote fibrosis of CFBs through the TGF-β/Smad signaling pathway and thus aggravate myocardial remodeling.
Published Version
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