A6: Impact of endothelial-derived lncRNAs for cardiomyocyte signal transduction and the cardiac stress response

Jörg Heineke

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Myocardial endothelial cells modulate the cardiac stress response in a paracrine manner and thereby exert a major impact on heart growth and function. While so far mainly endothelial derived protein growth factors were made responsible for these effects, we have now identified two endothelial derived, secreted long non-coding (lnc) RNAs that directly modulate signal-transduction in cardiomyocytes and induce cardiac hypertrophy and dysfunction. In this proposal, we are employing knock-out as well as endothelial specific overexpressing mice to decipher the role of these endothelial lncRNAs for cardiac growth and function during the cardiac response to stress. Furthermore, we are using cutting edge single cell kinase activity reporter and sequencing assays as well as RNA-binding protein discovery approaches to understand how these lncRNA target signal-transduction. We will also aim to discover and study novel lncRNAs that are secreted by endothelial cells and act on cardiomyocytes to impact cardiac growth and function.

Cardiomyocytes take up cardiac endothelial cell derived extracellular vesicles (EVs)

FACS staining of isolated primary cardiac endothelial cells

 

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