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Long non-coding RNAs acting as mediators

ESTIMATED READING TIME: 2 minutes

Congratulations to Merve Keles on obtaining her PhD from the Ruperto Carola University Heidelberg with the thesis “Secreted long non-coding RNAs Gadlor1 and Gadlor2 act as mediators of cardiac remodelling during pressure overload”, where TATAA’s RNA spikes were successfully used as exogeneous controls. The expression of Gadlor lncRNAs is significantly increased in mice after transverse aortic constriction (TAC), but also in the myocardium and the serum of patients suffering from chronic heart failure.

Abstract

Pathological cardiac overload triggers maladaptive myocardial remodelling that predisposes to the development of heart failure. The contribution of long non-coding RNAs (lncRNAs) to intercellular signalling during cardiac remodelling is largely unknown. In this study, two novel long non-coding RNAs, Gadlor1 and Gadlor2, which are enriched in endothelial-cell-derived extracellular vesicles (EVs) were described. The functional role of endogenous Gadlor lncRNAs was investigated in intra-cardiac communication during cardiac remodelling upon pressure overload.

Gadlor1 and Gadlor2 are novel long non-coding RNAs, which are upregulated in cardiac pathological overload and are secreted from endothelial cells within EVs. Gadlor1 and Gadlor2 induce cardiac dysfunction, cardiomyocyte hypertrophy and myocardial fibrosis by acting on multiple cardiac cells, affecting cellular gene expression and by affecting calcium dynamics in cardiomyocytes, which take up the Gadlor1/2 by EV-mediated transfer from endothelial cells. Targeted inhibition of Gadlor lncRNAs in endothelial cells or fibroblasts might serve as a therapeutic strategy in the future.

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