Key result
Knockdown of lncRNA Miat alleviated pirarubicin-induced cardiomyocyte injury by targeting and regulating miR-129-1-3p.
Why the study?
Pirarubicin is a widely used antitumor drug, but its cardiotoxicity limits its use, prompting investigation into the protective effect and mechanism of lncRNA Miat knockdown.
Does lncRNA Miat knockdown protect against pirarubicin-induced cardiotoxicity in immortalized mouse cardiomyocytes?
Does lncRNA Miat knockdown protect against pirarubicin-induced cardiotoxicity in immortalized mouse cardiomyocytes?
Knockdown of lncRNA Miat protects against pirarubicin-induced cardiotoxicity in vitro by targeting miR-129-1-3p, suggesting a potential therapeutic target for anthracycline-induced cardiotoxicity.
Should not change anthracycline cardiotoxicity management; hypothesis-generating for Miat targeting in preclinical models.
Pirarubicin (THP) is a widely used antitumor drug in clinical practice, but its cardiotoxicity limits its use. The aim of this study was to investigate the protective effect and mechanism of knockdown of lncRNA Miat in THP‐induced cardiotoxicity. The extent of damage to immortalized cardiomyocytes in mice was assessed by CCK8, TUNEL, ROS, Ca 2+ , RT‐qPCR, and Western blot. The relative levels of Miat in THP‐treated cardiomyocytes (HL‐1) were measured. The protective effect of Miat on THP‐treated HL‐1 was assessed. The binding relationship between lncRNA Miat and mmu‐miRNA‐129‐1‐3p was verified by a dual luciferase reporter gene assay. The protective role of Miat/miRNA‐129‐1‐3p in THP‐induced HL‐1 was explored by performing a rescue assay. THP reduced cell viability, induced apoptosis, triggered oxidative stress and calcium overload. Expression of Miat in HL‐1 was significantly elevated after THP treatment. Miat knockdown significantly alleviated the cardiotoxicity of THP. MiR‐129‐1‐3p is a direct target of Miat. Knockdown of miR‐129‐1‐3p reversed the protective effect of Miat knockdown on HL‐1. Miat knockdown can alleviate THP‐induced cardiomyocyte injury by regulating miR‐129‐1‐3p.
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Huang et al. (2023) studied Pirarubicin-induced cardiotoxicity. lncRNA Miat knockdown vs. Control / THP-treated cardiomyocytes without knockdown was evaluated on Cardiomyocyte injury (cell viability, apoptosis, oxidative stress, calcium overload). Knockdown of lncRNA Miat alleviated pirarubicin-induced cardiomyocyte injury by targeting and regulating miR-129-1-3p.
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