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Cmarr/miR-540-3p axis promotes cardiomyocyte maturation transition by orchestrating Dtna expression

ABSTRACT: Here, our study showed that a heart-rich lncRNA, Cmarr, which is specifically upregulated during heart development, promoted the maturation transition of ESC-CMs. Cmarr interacted with miR-540-3p to increase the expression of Dtna (a key component of DGC), thus served as a new regulator of the DGC-YAP complex and cardiomyocyte maturation. Our study further identified that Cmarr could recover Dtna expression in the MI heart and attenuate the cardiac remodeling.

ORGANISM(S): Mus musculus

PROVIDER: GSE158202 | GEO | 2022/03/01

REPOSITORIES: GEO

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Cmarr/miR-540-3p axis promotes cardiomyocyte maturation transition by orchestrating Dtna expression.

Project description:The immature phenotype of embryonic stem cell-derived cardiomyocytes (ESC-CMs) limits their application. However, the molecular mechanisms of cardiomyocyte maturation remain largely unexplored. This study found that overexpression of long noncoding RNA (lncRNA)-Cmarr, which was highly expressed in cardiomyocytes, promoted the maturation change and physiological maturation of mouse ESC-CMs (mESC-CMs). Moreover, transplantation of cardiac patch overexpressing Cmarr exhibited better retention of mESC-CMs, reduced infarct area by enhancing vascular density in the host heart, and improved cardiac function in mice after myocardial infarction. Mechanism studies identified that Cmarr acted as a competitive endogenous RNA to impede the repression of miR-540-3p on Dtna expression and promoted the binding of the dystrophin-glycoprotein complex (DGC) and yes-associated protein (YAP), which in turn reduced the proportion of nuclear YAP and the expression of YAP target genes. Therefore, this study revealed the function and mechanism of Cmarr in promoting cardiomyocyte maturation and provided a lncRNA that can be used as a functional factor in the construction of cardiac patches for the treatment of myocardial infarction.

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