Abstract
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-1β 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 up-regulating both GNAI2 and PCBP1 at a miR-556-5p dependent way.
Highlights
Endothelial cell (EC) dysfunction is regarded as an important marker for atherosclerosis at an early stage
The results depicted that secretion and protein expression of IL-6 and IL-1b were significantly enhanced in Oxidative low-density lipoprotein (ox-LDL)-induced human umbilical vein endothelial cells (HUVECs) than in the control group (Figures 1F, G)
Present study was designed to probe into the biological role of Small nucleolar RNA host gene 1 (SNHG1) which has been implicated in atherosclerosis-caused cerebral infraction and could regulate cardiovascular disorders
Summary
Endothelial cell (EC) dysfunction is regarded as an important marker for atherosclerosis at an early stage. Persistent adverse stimulations could lead to EC injury and apoptosis in atherosclerosis (Akhtar et al, 2015). Oxidative low-density lipoprotein (ox-LDL) can induce hyperlipemia and stimulate endothelial dysfunction and apoptosis via enhancing oxidative stress in ECs (Pandey et al, 2014). Inflammatory response induced by ox-LDL is verified as a key event in atherosclerosis though how ox-LDL induces EC injury is unknown, (Back et al, 2019). It is of great significance to explore the downstream molecular mechanism of ox-LDL-induced EC injury.
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