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Targeting JMJD3 histone demethylase mediates cardiac fibrosis and cardiac function following myocardial infarction.

Abstract：

:Myocardial fibrosis is the pathological consequence of injury-induced fibroblastto-myofibroblast transition, resulting in increased stiffness and diminished cardiac function. Histone modification has been shown to play an important role in the pathogenesis of cardiac fibrosis. Here, we identified H3K27me3 demethylase JMJD3/KDM6B promotes cardiac fibrosis via regulation of fibrogenic pathways. Using neonatal rat cardiac fibroblasts (NRCF), we show that the expression of endogenous JMJD3 is induced by angiotensin II (Ang II), while the principle extracellular matrix (ECM) such as fibronectin, CTGF, collagen I and III are increased. We find that JMJD3 inhibition markedly enhances the suppressive mark (H3K27me3) at the beta (β)-catenin promoter in activated cardiac fibroblasts, and then substantially decreases expression of fibrogenic gene. Both inhibition of β-catenin-mediated transcription with ICG-001 and genetic loss of β-catenin can prevent Ang II-induced ECM deposition. Most importantly, in vivo inhibition of JMJD3 rescues myocardial ischemia-induced cardiac fibrosis and cardiac dysfunction. Collectively, our findings are the first to report a novel role of histone demethylase JMJD3 in the pro-fibrotic cardiac fibroblast phenotype, pharmacological targeting of JMJD3 might represent a promising therapeutic approach for the treatment of human cardiac fibrosis and other fibrotic diseases.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Long F,Wang Q,Yang D,Zhu M,Wang J,Zhu Y,Liu X

doi

10.1016/j.bbrc.2020.05.115

subject

Has Abstract

pub_date

2020-08-06 00:00:00

pages

671-677

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(20)31037-8

journal_volume

528

pub_type

杂志文章

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