Abstract
BackgroundSCIRT has been characterized as a key player in cancer biology, while its role in other human diseases is unclear. This study explored its role in atherosclerosis, with a specific focus on its interaction with SCIRT and miR-146a.MethodsThe expression of SCIRT and miR-146a in atherosclerosis-affected tissues and healthy tissues from 56 atherosclerosis patients were analyzed by RT-qPCR. The expression of SCIRT in nuclear and cytoplasm samples was detected by RNA fractionation assay. The direct interaction between SCIRT and miR-146a was detected by RNA pull-down assay. SCIRT and miR-146a were overexpressed in human aortic smooth muscle cells (HAOSMCs) to study the crosstalk between them. The role of SCIRT and miR-146a in the proliferation of HAOSMCs was analyzed with BrdU assay.ResultsSCIRT was downregulated by atherosclerosis, while miR-146a was upregulated by atherosclerosis. SCIRT was detected in both cytoplasm and nuclear samples, and it directly interacted with miR-146a. In HAOSMCs, overexpression of SCIRT and miR-146a did not affect the expression of each other. Interestingly, SCIRT suppressed the proliferation of HAOSMCs and reduced the enhancing effects of miR-146a on cell proliferation.ConclusionTherefore, SCIRT is downregulated in atherosclerosis and it suppresses the proliferation of HAOSMCs by sponging miR-146a in cytoplasm.
Highlights
As a common chronic disease, atherosclerosis is caused by the formation of atheromatous plaque, which is mainly composed of cholesterol, fats and other substances [1, 2]
The results showed that SCIRT was significantly downregulated in atherosclerosis
We showed that SCIRT is downregulated in atherosclerosis and it may sponge miR-146a to suppress the proliferation of human aortic smooth muscle cells (HAOSMCs)
Summary
As a common chronic disease, atherosclerosis is caused by the formation of atheromatous plaque, which is mainly composed of cholesterol, fats and other substances [1, 2]. Atherosclerosis at early stages shows no symptoms [3]. Once severe conditions have developed, depending on the arteries that are affected, atherosclerosis may cause kidney problems, peripheral artery disease, stroke and coronary artery disease [4, 5]. With active treatment and the changing in lifestyle, early atherosclerosis may be reversible, while atherosclerosis in advanced stages still cannot be treated efficiently. SCIRT has been characterized as a key player in cancer biology, while its role in other human diseases is unclear. This study explored its role in atherosclerosis, with a specific focus on its interaction with SCIRT and miR-146a
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