Background: Myocardial ischemia/reperfusion (I/R) injury is a common pathophysiological change after myocardial reperfusion therapy. Recent research confirmed that long non-coding RNA (IncRNAs) played an important role in many cardiovascular diseases. This study was carried out to explore the role of lncRNA XR008038 in the I/R progression.
Methods: GSE103731 database was downloaded from NCBI Gene Expression Omnibus to analyze the differently expressed lncRNAs. Cell viability was determined by CCK-8 assay. Cell apoptosis was detected by flow cytometry and TUNEL staining. Northern blot and qRT-PCR was carried out to detect the XR008038 levels. The mitochondrial membrane potential was assessed by JC-1 staining. Western blot was conducted to measure the expression of apoptosis related proteins. RNA pull down and RIP assay was carried out to explore the relationship between XR008038 and galectin-3.
Results: The results showed that XR008038 was up-regulated in the H/R treated H9c2 cells and the myocardial tissues of the I/R rats. XR008038 silencing promoted the cell growth and mitochondrial membrane potential, inhibited the cell apoptosis of the H/R treated H9c2 cells. Additionally, the MDA content was decreased and SOD activity was enhanced in the H/R treated H9c2 cells and the myocardial tissues of the I/R rats after XR008038 knockdown. XR008038 interacted with galectin-3 and further regulated the mRNA stability of galectin-3. Galectin-3 overexpression neutralized the role of si-XR008038 in the H/R treated H9c2 cells.
Conclusion: In conclusion, XR008038 promoted the oxidative damage in I/R progression through regulating the galectin-3 levels.
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| http://dx.doi.org/10.1016/j.ijcard.2024.132955 | DOI Listing |
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