Abstract
The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes. In cultured human umbilical vein endothelial cells (HUVECs), the expression of miR-455-3p, eNOS protein and the NO production was detected after administration with 50 μM NaHS. The results indicated that H2S could augment the expression of miR-455-3p and eNOS protein, leading to the increase of NO level. We also found that overexpression of miR-455-3p in HUVECs increased the protein levels of eNOS whereas inhibition of miR-455-3p decreased it. Moreover, H2S and miR-455-3p could no longer increase the protein level of eNOS in the presence of proteasome inhibitor, MG-132. In vivo, miR-455-3p and eNOS expression were considerably increased in C57BL/6 mouse aorta, muscle and heart after administration with 50 μmol/kg/day NaHS for 7 days. We also identified that H2S levels and miR-455-3p expression increased in human atherosclerosis plaque while H2S levels decreased in plasma of atherosclerosis patients. Our data suggest that the stability of eNOS protein and the NO production could be regulated by H2S through miR-455-3p.
Highlights
The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase and nitric oxide (NO) production, and to identify the role of microRNA-455-3p during those processes
NO was first defined as an endothelial-derived relaxing factor, and is found to be highly relevant to cardiovascular health6. endothelial nitric oxide synthase (eNOS) and inducible NOS are both expressed in the vascular endothelial cells, they are main origins of the vascular NO and play important roles in the regulation of angiogenesis and the pathogenesis of atherosclerosis[7,8,9,10]
DNAJB12 and DNAJB14 belong to the HSP40 protein family, which has been shown to facilitate the proteasomal degradation of neuronal nitric oxide synthase through enhancing their ubiquitination[17]
Summary
The aims of the present study are to determine whether hydrogen sulfide (H2S) is involved in the expression of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production, and to identify the role of microRNA-455-3p (miR-455-3p) during those processes. In cultured human umbilical vein endothelial cells (HUVECs), the expression of miR-455-3p, eNOS protein and the NO production was detected after administration with 50 μM NaHS. The results indicated that H2S could augment the expression of miR-455-3p and eNOS protein, leading to the increase of NO level. To investigate whether miR-455-3p is a regulator of eNOS during the regulation of endothelial cell migration and atherosclerosis plaque formation could elucidate the mechanisms by which H2S exerts its beneficial effects on endothelium protection and provide experimental data for further clinical applications of H2S derivatives
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