Dysfunction of human endothelial cells is an important trigger for atherosclerosis. Oxidative low-density lipoprotein (ox-LDL) usually was used to stimulate the dysfunction of human umbilical vein endothelial cells (HUVECs). LncRNA SNHG1 (small nucleolar RNA host gene 1) is a cerebral infarction-associated gene. The present study was designed to investigate the role of SNHG1 in ox-LDL-induced HUVECs. Cell viability was evaluated by CCK-8 and MTT assay. Cell apoptosis was detected by flow cytometry analysis. Cell inflammatory response was evaluated by detecting LDH, IL-6, IL-1b levels. The results revealed that up-regulation of SNHG1 attenuated ox-LDL-induced cell injury and inflammatory response in HUVECs. Next, mechanism assays including RNA immunoprecipitation (RIP) assay, luciferase reporter assay, and RNA pull-down assay, helped us to identify the interaction between miR-556-5 and SNHG1. GNAI2 (G protein subunit alpha i2) and PCBP1 (poly(rC) binding protein 1) were identified as the downstream targets of miR-556-5p. SNHG1 regulated dysfunctions of ox-LDL-induced HUVECs via sponging miR-556-5p and up-regulating GNAI2 and PCBP1. SNHG1 attenuated cell injury and inflammatory response in ox-LDL-induced HUVECs via upregulating both GNAI2 and PCBP1 at a miR-556-5p dependent way.

Introduction MicroRNAs (miRNAs) are considered as crucial modulators in myocardial ischemia and reperfusion (I/R) injury. The present study aimed to investigate the expression and biological functions of miR-214-5p via targeting Fas ligand (FASLG) in I/R injury. Material and methods Lactate dehydrogenase, casein kinase, malondialdehyde assay, reactive oxygen species (ROS) detection and cell apoptosis analysis measured cell damage and cell apoptosis in H9c2 cells under hypoxia/reperfusion (H/R) treatment. Bioinformatics and dual luciferase reporter assays demonstrated the molecular mechanism of miR-214-5p in cardiac cells. 2,3,5-Triphenyltetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining and adenovirus injection were performed in I/R treated mice. Results The expression of miR-214-5p was decreased in H/R injured H9c2 cells compared with control cells ( p < 0.001). Overexpression of miR-214-5p reduced cell damage and apoptosis in H9c2 cells under H/R treatment ( p < 0.001). Further study revealed that FASLG was a target of miR-214-5p. Enhanced expression of FASLG attenuated the protective function of miR-214-5p in H9c2 cells subjected to H/R injury ( P < 0.001). Moreover, the elevated expression of miR-214-5p by adenovirus injection protected cardiac cells from I/R injury in mice ( n = 6/per group). Conclusions We found that miR-214-5p exerted a protective role in I/R injured cardiac cells by direct targeting FASLG in vitro and in vivo .