title: [Effect and potential mechanism of β3-adrenoceptor activation on fibrosis in cardiac fibroblast cell].
abstract: OBJECTIVE
  To observe the effect of β3 adrenergic receptor (β3-AR) on fibrosis in cardiac fibroblasts(CFBs) and explore the related mechanisms.
  
  
  METHODS
  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.
  
  
  RESULTS
  (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.
  
  
  CONCLUSIONS
  Activation of β3-AR may promote fibrosis of CFBs through the TGF-β/Smad signaling pathway and thus aggravate myocardial remodeling.
authors.affiliation: Department of Cardiology, First Affiliated Hospital, School of Medicine, Shihezi University, Shihezi 832008, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.forename: H
authors.initials: H
authors.lastname: Zhang
authors.forename: Y T
authors.initials: YT
authors.lastname: Ma
authors.forename: Y N
authors.initials: YN
authors.lastname: Yang
authors.forename: B D
authors.initials: BD
authors.lastname: Chen
authors.forename: M M
authors.initials: MM
authors.lastname: Ma
authors.forename: X L
authors.initials: XL
authors.lastname: Zhu
mesh_terms: D000804:Angiotensin II / Q000494:pharmacology; D002478:Cells, Cultured; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D005347:Fibroblasts / Q000166:cytology* / Q000473:pathology; D005355:Fibrosis; D006801:Humans; D009206:Myocardium / Q000166:cytology*; D022702:Receptors, Adrenergic, beta-3 / Q000378:metabolism*; D018125:Receptors, Transforming Growth Factor beta / Q000378:metabolism; D015398:Signal Transduction; D051899:Smad2 Protein / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000378:metabolism
chemical_list: D024042:Collagen Type I; D024061:Collagen Type III; D022702:Receptors, Adrenergic, beta-3; D018125:Receptors, Transforming Growth Factor beta; C497782:SMAD2 protein, human; D051899:Smad2 Protein; C508960:TGFB1 protein, human; D053773:Transforming Growth Factor beta1; D000804:Angiotensin II