Dataset Information

Circ_0001206 regulates miR-665/CRKL axis to alleviate hypoxia/reoxygenation-induced cardiomyocyte injury in myocardial infarction.

ABSTRACT:

Aims

Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)-induced injury of MI.

Methods and results

Hypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real-time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the stability. Cell counting kit-8 (CCK-8), western blot, TUNEL, and flow cytometry assays evaluated cell viability and cell apoptosis. RNA pull-down, RNA binding protein immunoprecipitation (RIP), and luciferase reporter assays explored the mechanisms underlying MI. All experimental data were presented with mean ± standard deviation (SD) and P < 0.05 indicated statistical significance. Circ_0001206 was low-expressed in H9C2 cells under H/R treatment. Circ_0001206 was formed by cyclization of CRK like proto-oncogene, adaptor protein (CRKL). Circ_0001206 overexpression promoted cell viability and inhibited cardiomyocyte apoptosis. It was confirmed that circ_0001206 regulated CRKL expression via acting as a competing endogenous RNA (ceRNA) of microRNA-665 (miR-665). CRKL played a protective role in MI.

Conclusions

Circ_0001206 regulates miR-665/CRKL axis to alleviate H/R-induced cardiomyocyte injury in MI. Our findings suggest that circ_0001206 might be a potential target for MI treatment.

SUBMITTER: Wang D

PROVIDER: S-EPMC8934946 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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Publications

Circ_0001206 regulates miR-665/CRKL axis to alleviate hypoxia/reoxygenation-induced cardiomyocyte injury in myocardial infarction.

Wang Dongmei D Tian Limei L Wang Yan Y Gao Xiaoli X Tang Hanbo H Ge Junbo J

ESC heart failure 20220113 2

<h4>Aims</h4>Myocardial infarction (MI) is a type of cardiovascular disease caused by myocardial necrosis. Growing evidences have suggested that circular RNAs (circRNAs) play crucial roles in cardiac hypoxia/reoxygenation (H/R)-induced injury of MI.<h4>Methods and results</h4>Hypoxia/reoxygenation model of H9C2 cells was established and circ_0001206 expression was detected via quantitative real-time polymerase chain reaction. Ribonuclease R (RNase R) and Actinomycin D (Act D) assays verified the ...[more]

PMID: 35023295

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Project description:BackgroundAnesthetic postconditioning is a cellular protective approach whereby exposure to a volatile anesthetic renders a tissue more resistant to subsequent ischemic/reperfusion event. Sevoflurane postconditioning (SPostC) has been shown to exert cardioprotection against ischemia/reperfusion injury, but the underlying mechanism is unclear. We hypothesized that SPostC protects cardiomyocytes against hypoxia/reoxygenation (H/R) injury by maintaining/restoring mitochondrial morphological integrity, a critical determinant of cell fate.MethodsPrimary cultures of neonatal rat cardiomyocytes (NCMs) were subjected to H/R injury (3 h of hypoxia followed by 3 h reoxygenation). Intervention with SPostC (2.4% sevoflurane) was administered for 15 min upon the onset of reoxygenation. Cell viability, Lactate dehydrogenase (LDH) level, cell death, mitochondrial morphology, mitochondrial membrane potential and mitochondrial permeability transition pore (mPTP) opening were assessed after intervention. Mitochondrial fusion and fission regulating proteins (Drp1, Fis1, Mfn1, Mfn2 and Opa1) were assessed by immunofluorescence staining and western blotting was performed to determine the level of protein expression.ResultsCardiomyocyte H/R injury resulted in significant increases in LDH release and cell death that were concomitant with reduced cell viability and reduced mitochondrial interconnectivity (mean area/perimeter ratio) and mitochondrial elongation, and with reduced mitochondrial membrane potential and increased mPTP opening. All the above changes were significantly attenuated by SPostC. Furthermore, H/R resulted in significant reductions in mitochondrial fusion proteins Mfn1, Mfn2 and Opa1 and significant enhancement of fission proteins Drp1 and Fis1. SPostC significantly enhanced Mfn2 and Opa1 and reduced Drp1, without significant impact on Mfn1 and Fis1.ConclusionsSevoflurane postconditioning attenuates cardiomyocytes hypoxia/reoxygenation injury (HRI) by restoring mitochondrial fusion/fission balance and morphology.

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Dataset Information

Circ_0001206 regulates miR-665/CRKL axis to alleviate hypoxia/reoxygenation-induced cardiomyocyte injury in myocardial infarction.

Aims

Methods and results

Conclusions

Publications

Circ_0001206 regulates miR-665/CRKL axis to alleviate hypoxia/reoxygenation-induced cardiomyocyte injury in myocardial infarction.

Similar Datasets

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