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Abstract
BackgroundThis study focused on the roles of lncRNA THRIL in coronary atherosclerotic heart disease (CAD) through regulating AKT signaling pathway and directly interacting with FUS.MethodsQRT-PCR was conducted to detect the expression of THRIL in CAD blood samples and endothelial progenitor cells (EPCs). Cell autophagy of EPCs was examined through Cyto-ID Autophagy Detection Kit. CCK-8 assay and flow cytometry were carried out to assess cell viability and apoptosis under various interference conditions. Western blotting was conducted to detect the expression of interest proteins. The expression levels of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) were measured by qRT-PCR. The direct interactions between HCG18 and FUS was confirmed through RNA electrophoretic mobility shift assay (RNA EMSA) and RNA immunoprecipitation (RIP) assay.ResultsTHRIL was upregulated in CAD blood samples and EPCs. Knockdown of THRIL in EPCs promoted cell viability, inhibited cell autophagy and further suppressed the development of CAD. Over-expression of THRIL induced inactivation of AKT pathway, while knockdown of THRIL played reversed effects. THRIL directly interacted with FUS protein and knockdown of FUS reversed the over-expressing effect of THRIL on cell proliferation, autophagy and the status of AKT pathway.ConclusionTHRIL inhibits the proliferation and mediates autophagy of endothelial progenitor cells via AKT pathway and FUS.
Highlights
Coronary atherosclerotic heart disease (CAD) is one of the chronic diseases with very high mortality rate due to the acceleration of population aging process (CorralDebrinski et al, 1992)
LncRNA THRIL was up-regulated in coronary atherosclerotic heart disease (CAD) blood samples and inhibits the proliferation of endothelial progenitor cells (EPCs) To detect the expression of THRIL, qRT-PCR was conducted and the results showed that the expression levels of THRIL were greatly enhanced in CAD blood and EPC (P < 0.01, Fig. 1a)
cell counting kit-8 (CCK-8) assay revealed that THRIL shRNA promoted cell viability of EPCs in CAD and pCMV6-THRIL obviously inhibited cell viability compared with that in Negative control (NC) (P < 0.01, Fig. 1c)
Summary
Coronary atherosclerotic heart disease (CAD) is one of the chronic diseases with very high mortality rate due to the acceleration of population aging process (CorralDebrinski et al, 1992). The incidence of CAD and the resulting social and economic burden are increasing (Ornish et al, 1990). Cruuent treatments such as medical treatment, percutaneous coronary intervention (PCI), and coronary artery bypass surgery. Endothelial progenitor cells (EPC) differentiate into endothelial cells (EC) and participate in endothelium recovery, new blood vessels formation, and suppression of atherosclerosis (Zhang et al, 2014). This study focused on the roles of lncRNA THRIL in coronary atherosclerotic heart disease (CAD) through regulating AKT signaling pathway and directly interacting with FUS
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