LINC01278 Sponges miR‐500b‐5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection

Apr 29, 2021Journal of the American Heart Association

LINC01278 controls changes in human blood vessel muscle cells during aortic dissection by regulating ACTG2 through miR-500b-5p

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Abstract

In a comparison of 6 aortic dissection samples and 6 control samples, linc01278 and ACTG2 were found to be downregulated, while miR-500b-5p was upregulated in aortic dissection tissues.

Linc01278, microRNA-500b-5p, and ACTG2 are involved in the vascular smooth muscle contraction pathway.
Molecular markers associated with VSMC phenotypic switching, such as SM22α, SMA, calponin, and MYH11, were downregulated in aortic dissection tissues.
Overexpression of linc01278 reduced VSMC proliferation and phenotypic switching, while its downregulation had the opposite effect.
Linc01278 was confirmed to regulate miR-500b-5p, which directly targets ACTG2 in HEK293T cells.
The linc01278-miR-500b-5p-ACTG2 axis may serve as a basis for developing diagnostic markers and therapeutic targets for aortic dissection.

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Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. We integrated the mRNA microarray data set with GSE52093 to determine the differentially expressed genes. Bioinformatic analysis, including Gene Expression Omnibus 2R, Venn diagram analysis, gene ontology, pathway enrichment, and protein-protein interaction networks were used to identify the target lncRNA, microRNA, and mRNA involved in AD. Subsequently, we validated the bioinformatics data using techniques in molecular biology in human tissues and VSMCs. Linc01278, microRNA-500b-5p, and ACTG2 played an important role in the vascular smooth muscle contraction pathway. Linc01278 and ACTG2 were downregulated and miR-500b-5p was upregulated in AD tissues. Molecular markers of VSMC phenotypic switching, including SM22α, SMA, calponin, and MYH11, were downregulated in AD tissues. Plasmid-based overexpression and RNA interference-mediated downregulation of linc01278 weakened and enhanced VSMC proliferation and phenotypic switching, respectively. Dual-luciferase reporter assays confirmed that linc01278 regulated miR-500b-5p that directly targeted ACTG2 in HEK293T cells. Conclusions These data demonstrate that linc01278 regulates ACTG2 to control the phenotypic switch in VSMCs by sponging miR-500b-5p. This linc01278-miR-500b-5p-ACTG2 axis has a potential role in developing diagnostic markers and therapeutic targets for AD.

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LINC01278 Sponges miR‐500b‐5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection

Abstract

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