title: Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1.
abstract: OBJECTIVE
  Sonodynamic therapy (SDT) is a localized ultrasound-activated therapy for atherosclerosis when combined with a sonosensitizer, 5-aminolevulinic acid (ALA), but whether it can prevent cardiac fibrosis has not been studied. In the present study, we evaluated the effects SDT on fibrogenesis in rat cardiac fibroblasts.
  
  
  METHODS
  The primary cardiac fibroblasts were isolated from rats, and induced to fibrogenesis with TGF-β1. With this in vitro model, we tested the preventive effects of SDT on fibrogenesis and further the underlying mechanism.
  
  
  RESULTS
  TGF-β1 stimulation up-regulated α-SMA and COLI/III protein levels in cardiac fibroblasts, and enhanced the progression of cells from the G0/G1 phase to the S phase. SDT inhibited the TGF-β1 mediated cell proliferation and decreased the levels of α-SMA and COLI/III by activating AKT/GSK3β pathway and blocking TGF-β1/SMAD3 signaling.
  
  
  CONCLUSIONS
  Our studies demonstrate an antifibrotic effect of SDT in rat cardiac fibroblasts, suggesting that SDT may intervene cardiac fibrogenesis by regulating myocardial fibrotic remodeling.
authors.affiliation: Department of Cardiology, the First Affiliated Hospital of Harbin Medical University, Harbin, P. R. China.
authors.forename: Yuanyuan
authors.initials: Y
authors.lastname: Guo
authors.forename: Zengxiang
authors.initials: Z
authors.lastname: Dong
authors.forename: Yuanqi
authors.initials: Y
authors.lastname: Shi
authors.forename: Wei
authors.initials: W
authors.lastname: Wang
authors.forename: Lu
authors.initials: L
authors.lastname: Wang
authors.forename: Jing
authors.initials: J
authors.lastname: Sun
authors.forename: Xin
authors.initials: X
authors.lastname: Sun
authors.forename: Zhen
authors.initials: Z
authors.lastname: Tian
authors.forename: Jianting
authors.initials: J
authors.lastname: Yao
authors.forename: Zhitao
authors.initials: Z
authors.lastname: Li
authors.forename: Jiali
authors.initials: J
authors.lastname: Cheng
authors.forename: Ye
authors.initials: Y
authors.lastname: Tian
mesh_terms: D000622:Aminolevulinic Acid / Q000494:pharmacology; D000818:Animals; D000831:Animals, Newborn; D002453:Cell Cycle / Q000187:drug effects; D016923:Cell Death / Q000187:drug effects; D002461:Cell Line, Transformed; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D003094:Collagen / Q000096:biosynthesis; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism / Q000473:pathology*; D005355:Fibrosis; D000071679:Glycogen Synthase Kinase 3 beta / Q000378:metabolism; D042541:Intracellular Space / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D010766:Phosphorylation / Q000187:drug effects; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011524:Protoporphyrins / Q000494:pharmacology; D017207:Rats, Sprague-Dawley; D051900:Smad3 Protein / Q000378:metabolism; D053773:Transforming Growth Factor beta1 / Q000494:pharmacology*; D014465:Ultrasonics
chemical_list: D011524:Protoporphyrins; D051900:Smad3 Protein; D053773:Transforming Growth Factor beta1; D000622:Aminolevulinic Acid; D003094:Collagen; C028025:protoporphyrin IX; D000071679:Glycogen Synthase Kinase 3 beta; D051057:Proto-Oncogene Proteins c-akt