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Introduction

Endothelium dysfunction plays a critical role in atherosclerosis. MicroRNAs are endogenous non-coding RNAs that suppress gene expression by binding to the 3' untranslated regions of target genes. MiR-495 can regulate the proliferation and apoptosis of cancer cells, however, the roles of miR-495 in endothelial cells (ECs) remain unclear. Therefore, this study aims to investigate the roles and mechanisms of miR-495 on ECs proliferation and apoptosis.

Materials and methods

MiR-495 and CCL2 expressions were examined using quantitative RT-PCR, ELISA assay and western blot. Bioinformatics analysis and luciferase reporter assay were used to examine the regulatory relationship between miR-495 and CCL2. CCK8 assay, BrdU incorporation assay and flow cytometry were used to analyze the roles of miR-495 and CCL2 on the proliferation of human umbilical vein endothelial cells (HUVECs). The effects of miR-495 and CCL2 on HUVECs apoptosis were examined by tunnel staining and western blot.

Results

MiR-495 was down-regulated in patients with coronary artery disease compared with healthy controls. CCL2 was a novel target gene of miR-495. MiR-495 significantly promoted HUVECs proliferation by altering cell cycle distribution, and it also inhibited HUVECs apoptosis by affecting the expression of cleaved caspase 3. Effects of miR-495 on HUVECs proliferation and apoptosis were significantly reversed by overexpression of CCL2.

Conclusions

MiR-495 could affect HUVECs proliferation and apoptosis by directly targeting CCL2. This is the first report to disclose the roles and mechanisms of miR-495 on HUVECs proliferation and apoptosis, which may provide a theoretical basis for clarifying the mechanisms of atherosclerosis."xsd:string
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http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Liu D."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Li Y."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Zhang X.L."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Zhu N."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Peng C.F."xsd:string
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http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Yan C.H."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Han Y.L."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/author"Rong J.J."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/date"2015"xsd:gYear
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/name"Thromb Res"xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/pages"146-154"xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/title"MicroRNA-495 regulates the proliferation and apoptosis of human umbilical vein endothelial cells by targeting chemokine CCL2."xsd:string
http://purl.uniprot.org/citations/25466836http://purl.uniprot.org/core/volume"135"xsd:string
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