ArticleMolecular and cellular biochemistry2022
LncRNA XIST facilitates hypoxia-induced myocardial cell injury through targeting miR-191-5p/TRAF3 axis.
Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 11 citations in OpenAlex.
- KLF9 aggravates the cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy through the lncRNA UCA1/p27 axis.International journal of experimental pathology · 2025Article
- Screening and validation of key microRNAs regulating muscle development in Hanper sheep.PloS one · 2025Article
- Serum MicroRNA-191-5p Levels in Vascular Complications of Type 1 Diabetes: The EURODIAB Prospective Complications Study.The Journal of clinical endocrinology and metabolism · 2023Article
- LOXL1-AS1 Aggravates Myocardial Ischemia/Reperfusion Injury Through the miR-761/PTEN Axis.Korean circulation journal · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
Myocardial infarction is one of the most lethal diseases in cardiovascular diseases. In the present work, we aimed to elucidate the molecular and functional association long non-coding RNA (lncRNA) X-inactive specific transcript (XIST), microRNA (miR)-191-5p, and TNF receptor-associated factor 3 (TRAF3). Human cardiomyocyte primary cells (HCMs) were stimulated by hypoxia to establish a model of myocardial injury in vitro. The relative expressions of XIST, miR-191-5p, and TRAF3 were measured using quantitative real-time polymerase chain reaction (qRT-PCR) assay. The capabilities of proliferation and apoptosis were determined using cell counting kit (CCK-8) and flow cytometry assays, respectively. The molecular interactions were verified using dual luciferase assay. The protein contents of TRAF3, Bcl-2, and Bax were calculated using western blot assay. XIST was significantly increased, but miR-191-5p was reduced in hypoxia-treated HCMs compared to that in control group. Either downregulated XIST or enforced miR-191-5p markedly enhanced cell viability and restrained cell apoptotic rate in hypoxia-treated HCMs. Mechanistically, XIST directly interacted with miR-191-5p to competitive releasing TRAF3 expression. Importantly, overexpression of TRAF3 dramatically diminished the protective effects of XIST knockdown on hypoxia-triggered HCMs injury. Collectively, our data elucidated a novel "lncRNA XIST/miR-191-5p/TRAF3" molecular network in vitro, indicating that the reduced lncRNA XIST-protected HCMs from hypoxia-induced cell injury by regulating miR-191-5p/TRAF3 signaling, which might provide some convincing evidences for further understanding the influences of "lncRNA-miRNA-mRNA" network in the development of MI.
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