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LncRNA-HOTAIR Inhibits H9c2 Apoptosis After Acute Myocardial Infarction via miR-206/FN1 Axis

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Abstract

Although previous studies showed that long non-coding RNAs (lncRNAs) have critical roles in the pathogenesis of acute myocardial infarction (AMI), the underlying molecular mechanism that lncRNAs participate in MI remains unclear. Herein, we explored the expression of lncRNA HOX antisense non-coding RNA (HOTAIR) in the serum of MI patients and mouse model of AMI. Biological functions of HOTAIR in hypoxic H9c2 cells, the in vitro model of MI, were also assessed. RT-qPCR results showed that HOTAIR expression was downregulated in the serum of AMI patients and AMI mice. HOTAIR overexpression promoted H9c2 cell viability and inhibited cell apoptosis under hypoxic conditions. Mechanically, HOTAIR was regulated by miR-206 and FN1 was the direct target of miR-206. More importantly, miR-206 overexpression or FN1 knockdown reversed the effect of HOTAIR overexpression on H9c2 cell viability and apoptosis under hypoxic conditions. Therefore, targeting the HOTAIR/miR-206/FN1 axis may be a promising therapeutic method for MI.

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Data Availability

All data collection and analysis were conducted under double blind conditions and were supported by the Funing County People’s Hospital. We will provide the original data at any time if necessary.

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Acknowledgements

The present study was supported by the Funing County People’s Hospital.

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GZ conceived and designed the experiments, JY analyzed and interpreted the results of the experiments, and RM and CW performed the experiments.

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Correspondence to Guisheng Zhao.

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The authors declare no competing interests.

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All experimental procedures involving animals have followed the standard ethical guidelines of the Ethical Committee of the Funing County People’s Hospital.

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Yao, J., Ma, R., Wang, C. et al. LncRNA-HOTAIR Inhibits H9c2 Apoptosis After Acute Myocardial Infarction via miR-206/FN1 Axis. Biochem Genet 60, 1781–1792 (2022). https://doi.org/10.1007/s10528-022-10185-9

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