Long non‑coding RNA MEG3 knockdown alleviates hypoxia‑induced injury in rat cardiomyocytes via the miR‑325‑3p/TRPV4 axis.

Acute myocardial infarction (AMI) is a common cardiac disease. Long non‑coding RNA maternally expressed 3 (MEG3) is associated with cellular processes in numerous complicated diseases, including AMI. However, the mechanism underlying MEG3 in myocardial hypoxia is not completely understood. The present study aimed to investigate the underlying mechanism of MEG3 in myocardial hypoxia. The expression levels of hypoxia‑inducible factor 1α (HIF1α), MEG3, microRNA (miR)‑325‑3p, and transient receptor potential cation channel subfamily V member 4 (TRPV4) in hypoxia‑treated H9c2 cells were detected via reverse transcription‑quantitative PCR. The protein expression levels of HIF1α, Bcl‑2, Bax, cleaved caspase‑3 and TRPV4 were detected via western blotting. Cell viability and apoptosis were assessed by performing an MTT assay and flow cytometry, respectively. Lactate dehydrogenase (LDH) release was monitored by conducting an LDH determination assay. The dual‑luciferase reporter assay was performed to verify the targeted relationship between miR‑325‑3p and MEG3 or TRPV4. The expression levels of MEG3 and TRPV4 were significantly increased, whereas miR‑325‑3p expression levels were significantly decreased in hypoxic H9c2 cells compared with normoxic H9c2 cells. In addition, miR‑325‑3p was downregulated by MEG3 compared with the vector group, and miR‑325‑3p targeted TRPV4 in hypoxia‑treated H9c2 cells. The results indicated that MEG3 knockdown attenuated hypoxia‑stimulated injury in H9c2 cells by regulating miR‑325‑3p. TRPV4 knockdown also mitigated hypoxia‑induced injury in H9c2 cells via miR‑325‑3p. Furthermore, compared with the vector group, MEG3 increased TRPV4 expression in hypoxia‑treated H9c2 cells by sponging miR‑325‑3p. Collectively, the results of the present study suggested that MEG3 modulated TRPV4 expression to aggravate hypoxia‑induced injury in rat cardiomyocytes by sponging miR‑325‑3p.