4.4 Article

LncRNA TONSL-AS1 participates in coronary artery disease by interacting with miR-197

Journal

MICROVASCULAR RESEARCH
Volume 136, Issue -, Pages -

Publisher

ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mvr.2021.104152

Keywords

Coronary artery disease; TONSL-AS1; miR-197; Apoptosis

Funding

  1. Health Commission of Hubei Province Scientific Research Project [WJ2021M006]

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This study found significant differences in HDL-C, LDL-C, and gensini score in patients with CAD. TONSL-AS1 was downregulated in CAD, and low expression levels of TONSL-AS1 and high expression levels of miR-197 predicted poor survival of CAD patients. Overexpression of TONSL-AS1 attenuated the effects of overexpression of miR-197 on migration and apoptosis of HCAECs.
Background: It has been reported that high expression levels of miR-197 can predict coronary artery disease (CAD). Our bioinformatics analysis showed that miR-197 may bind to long non-coding RNA (lncRNA) TONSLAS1. This study aimed to investigate the role of TONSL-AS1 in CAD. Methods: This study included 60 CAD patients and 60 healthy controls. Coronary angiography was performed to diagnose CAD. The interaction between TONSL-AS1 and miR-197 was predicted by IntaRNA2.0. Western-blot analysis was performed to illustrate the effect of MTONSL-AS1, miR-197 and BCL2 on human primary coronary artery endothelial cells (HCAECs). Cell migration assay was performed to explore the roles of MTONSL-AS1, miR-197 and BCL2 in regulating cell migration. Cell apoptosis assay was performed to investigate the role of MTONSL-AS1, miR-197 and BCL2 in regulating the apoptosis of HCAECs. Result: Significant differences in high-density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), and gensini score were observed in patients with CAD. In addition, TONSL-AS1 was downregulated in CAD. Follow-up study revealed that low expression levels of TONSL-AS1 and high expression levels of miR-197 predicted poor survival of CAD patients. Overexpression experiments showed that TONSL-AS1 and miR-197 had no significant effect on the expression of each other. We speculated that MAFG-AS1 may sponge miR-145. Moreover, overexpression of TONSL-AS1 increased, while overexpression of miR-197 decreased the expression levels of BCL2. Furthermore, overexpression of TONSL-AS1 attenuated the effects of overexpression of miR-197 on migration and apoptosis of HCAECs. Conclusions: Therefore, the expression of TONSL-AS1 predicted the survival of CAD patients and it sponged miR197 to inhibit the apoptosis of HCAECs.

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