BNIP3L promotes cardiac fibrosis in cardiac fibroblasts through [Ca(2+)]i-TGF-β-Smad2/3 pathway

Scientific Reports
Weili LiuLingjia Qian

Abstract

Fibrosis is an important, structurally damaging event that occurs in pathological cardiac remodeling, leading to cardiac dysfunction. BNIP3L is up-regulated in pressure overload-induced heart failure and has been reported to play an important role in cardiomyocyte apoptosis; however, its involvement in cardiac fibroblasts (CFs) remains unknown. We prove for the first time that the expression of BNIP3L is significantly increased in the CFs of rats undergoing pressure overload-induced heart failure. Furthermore, this increased BNIP3L expression was confirmed in cultured neonatal rat CFs undergoing proliferation and extracellular matrix (ECM) protein over-expression that was induced by norepinephrine (NE). The overexpression or suppression of BNIP3L promoted or inhibited NE-induced proliferation and ECM expression in CFs, respectively. In addition, [Ca(2+)]i, transforming growth factor beta (TGF-β) and the nuclear accumulation of Smad2/3 were successively increased when BNIP3L was overexpressed and reduced when BNIP3L was inhibited. Furthermore, the down-regulation of TGF-β by TGF-β-siRNA attenuated the increase of BNIP3L-induced fibronectin expression. We also demonstrated that the increase of BNIP3L in CFs was regulated by NE-AR...Continue Reading

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Citations

Feb 19, 2020·Dermatologic Therapy·Agata KrawczykJoanna Gola
Jun 7, 2019·Liver International : Official Journal of the International Association for the Study of the Liver·Stefania Di MauroSalvatore Piro
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Methods Mentioned

BETA
transfection
FACS
flow cytometry
flow
nuclear translocation
Co-immunoprecipitation
electrophoresis

Software Mentioned

CELLQuest
ModFit LT
Image
ModFit
- Quant TL

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