circUBAP2 ameliorates hypoxia-induced acute myocardial injury by competing with miR-148b-3p and mediating CDKN1B expression

Graphical abstract

circUBAP2 ameliorates hypoxia-induced acute myocardial injury by competing with miR-148b-3p and mediating CDKN1B expression
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Keywords

Acute myocardial infarction
CCK-8 assay
CDKN1B
circUBAP2
Flow cytometry
High-throughput sequencing
Inflammation
LDH release
Luciferase activity
miR-148b-3p
RIP assay

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How to Cite

1.
Li F, Xu L, Ou J, Yang Z, Dai Y, Qiu M, Hou X, Zhu D. circUBAP2 ameliorates hypoxia-induced acute myocardial injury by competing with miR-148b-3p and mediating CDKN1B expression. Electron. J. Biotechnol. [Internet]. 2024 Mar. 15 [cited 2024 Nov. 21];68:1-10. Available from: https://www.ejbiotechnology.info/index.php/ejbiotechnology/article/view/2352

Abstract

Background: A recent high-throughput sequencing study revealed an anomalous underexpression of circular RNA UBAP2 (circUBAP2) in acute myocardial infarction (AMI), yet its biological function within this context remains elusive. This study aims to unravel whether circUBAP2 is instrumental in modulating the pathogenesis of AMI and to illuminate the underlying molecular mechanisms at play.

Results: circUBAP2 was abnormally low expressed in AMI. Inducing circUBAP2 ameliorated hypoxia-induced myocardial cell injury by enhancing cellular viability, and decreasing lactate dehydrogenase release, apoptosis, inflammation, and oxidative damage. circUBAP2 targeted miR-148b-3p, miR-148b-3p overexpression offset circUBAP2-induced cardioprotection. Cyclin-dependent kinase inhibitor 1B (CDKN1B) was mediated by miR-148b-3p, and CDKN1B upregulation suppressed the deleterious effect of circUBAP2 silencing on hypoxic AC16 cells. In addition, overexpression of circUBAP2 improved myocardial injury, decreased myocardial cell apoptosis, and alleviated inflammation and oxidative stress in AMI mice.

Conclusions: circUBAP2 ameliorates AMI by competitively binding to miR-148b-3p and mediating CDKN1B expression.

https://doi.org/10.1016/j.ejbt.2023.11.003
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References

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