We previously found that endothelial progenitor cell (EPC) exosomes prevent endothelial dysfunction and lung injury in sepsis in part due to their encapsulation of miRNA-126.
The aim of the study was to investigate whether miR-126, a regulator of MAPK signaling via targeting sprouty-related EVH1 domain-containing protein 1 (<i>SPRED1</i>) mRNA, is involved in the process by which icariside II (ICA II) ameliorates endothelial dysfunction in human cavernous endothelial cells (hCECs) exposed to a diabetic-like environment.
We show for the first time that circulating CD62E<sup>+</sup> MPs level and miR-126-3p content in MPs are abnormal in subjects with pre-diabetes; the content of miR-126-3p correlates with markers of endothelial inflammation, such as VCAM-1, plasma antioxidant capacity, and microparticles, well-accepted markers of endothelial dysfunction.
In conclusion, the present study shows that HDL isolated from CHF patients (NYHA-III) reduces the expression of pro-angiogenic miRs (i.e. miR-126 and miR-21), which may contribute to atherogenesis and endothelial dysfunction.