Sonodynamic Therapy Inhibits Fibrogenesis in Rat Cardiac Fibroblasts Induced by TGF-β1

Autor: Wei Wang, Xin Sun, Jianting Yao, Jiali Cheng, Jing Sun, Yuan-Qi Shi, Zengxiang Dong, Lu Wang, Zhen Tian, Yuanyuan Guo, Zhitao Li, Ye Tian
Jazyk: angličtina
Rok vydání: 2016
Předmět:
0301 basic medicine
Physiology
Cardiac fibrosis
Intracellular Space
Protoporphyrins
Stimulation
lcsh:Physiology
Rats
Sprague-Dawley

0302 clinical medicine
Fibrosis
TGF-β1
Ultrasonics
lcsh:QD415-436
Phosphorylation
SDT
Cell Line
Transformed

Cell Death
lcsh:QP1-981
Cell Cycle
030220 oncology & carcinogenesis
Collagen
medicine.medical_specialty
Cell Survival
Cardiac fibroblast
Transforming Growth Factor beta1
lcsh:Biochemistry
03 medical and health sciences
Internal medicine
medicine
Animals
Smad3 Protein
Protein kinase B
Cell Proliferation
Glycogen Synthase Kinase 3 beta
business.industry
Cell growth
Myocardium
AKT
Sonodynamic therapy
GSK3β
Aminolevulinic Acid
Fibroblasts
medicine.disease
030104 developmental biology
Endocrinology
Animals
Newborn

Cell culture
Cancer research
business
Proto-Oncogene Proteins c-akt
Transforming growth factor
Zdroj: Cellular Physiology and Biochemistry, Vol 40, Iss 3-4, Pp 579-588 (2016)
ISSN: 1421-9778
1015-8987
Popis: Background/Aims: 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. Conclusion: Our studies demonstrate an antifibrotic effect of SDT in rat cardiac fibroblasts, suggesting that SDT may intervene cardiac fibrogenesis by regulating myocardial fibrotic remodeling.
Databáze: OpenAIRE