Abstract
Cardiomyocytes (CMs) and endothelial cells (ECs) have an intimate anatomical relationship that is essential for maintaining normal development and function in the heart. Little is known about the mechanisms that regulate cardiac and endothelial crosstalk, particularly in situations of acute stress when local active processes are required to regulate endothelial function. We examined whether CM-derived exosomes could modulate endothelial function. Under conditions of glucose deprivation, immortalized H9C2 cardiomyocytes increase their secretion of exosomes. CM-derived exosomes are loaded with a broad repertoire of miRNA and proteins in a glucose availability-dependent manner. Gene Ontology (GO) analysis of exosome cargo molecules identified an enrichment of biological process that could alter EC activity. We observed that addition of CM-derived exosomes to ECs induced changes in transcriptional activity of pro-angiogenic genes. Finally, we demonstrated that incubation of H9C2-derived exosomes with ECs induced proliferation and angiogenesis in the latter. Thus, exosome-mediated communication between CM and EC establishes a functional relationship that could have potential implications for the induction of local neovascularization during acute situations such as cardiac injury.
Highlights
Cell-cell communication is crucial for normal functioning and coordination of cellular events in all tissues
We find that H9C2 cardiomyoblasts increase their exosome secretion under glucose starvation conditions
To study exosomes under stress conditions, we obtained “unpurified exosomes” (U exosomes) from H9C2 myoblasts cultured for 48 h in control (-St) or glucose starvation (+St) medium and examined their shape and average size by electron microscopy
Summary
Cell-cell communication is crucial for normal functioning and coordination of cellular events in all tissues. Cardiomyocytes (CMs) and endothelial cells (ECs) represent the most abundant cell types. The bulk of cardiac tissue mass corresponds to CMs, the number of myocardial ECs exceeds CMs by 3:1 [1, 2]. The intimate anatomical arrangement of these two cell types in the myocardium guarantees the optimal diffusion of oxygen and nutrients from the microvascular lumen through ECs to CMs. Several studies have shown that ECs affect cardiac performance [3] and, in return, CMs modulate EC function [4]. Several studies have shown that ECs affect cardiac performance [3] and, in return, CMs modulate EC function [4] Whether this intercellular communication pathway functions in acute stress situations is unknown
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