BEX1 is an RNA-dependent mediator of cardiomyopathy

Federica Accornero (), Tobias G. Schips, Jennifer M. Petrosino, Shan-Qing Gu, Onur Kanisicak, Jop H. Berlo and Jeffery D. Molkentin ()
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Federica Accornero: Cincinnati Children’s Hospital Medical Center
Tobias G. Schips: Cincinnati Children’s Hospital Medical Center
Jennifer M. Petrosino: Dorothy M. Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, Ohio State University
Shan-Qing Gu: Dorothy M. Davis Heart and Lung Research Institute, Department of Physiology and Cell Biology, Ohio State University
Onur Kanisicak: Cincinnati Children’s Hospital Medical Center
Jop H. Berlo: Cincinnati Children’s Hospital Medical Center
Jeffery D. Molkentin: Cincinnati Children’s Hospital Medical Center

Nature Communications, 2017, vol. 8, issue 1, 1-11

Abstract: Abstract Regulation of mRNA splicing, processing and stability is increasingly recognized as a critical control point in dynamically altering gene expression during stress or disease. Very little is understood of this process in heart failure. Here, we show that BEX1 is a heart failure-induced gene functioning as an mRNA-associated protein that enhances expression of a subset of cardiac disease-promoting genes. Modeling the increase in BEX1 that occurs in disease, cardiac-specific BEX1 transgenic mice show worse cardiac disease with stress stimulation, whereas Bex1 gene-deleted mice are protected from heart failure-promoting insults. Proteomic and interactive screening assays show that BEX1 is part of a large ribonucleoprotein processing complex involved in regulating proinflammatory mRNA expression in the heart. Specifically, induction of BEX1 augments the stability and expression of AU-rich element containing mRNAs typically found within proinflammatory genes. Thus, BEX1 functions as an mRNA-dependent effector that augments pathology-promoting gene expression during heart failure.

Date: 2017
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DOI: 10.1038/s41467-017-02005-1

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