Key result
MIAT knockdown restores cardiac contractile function post-MI by preventing TSPO-mediated mitochondrial damage.
Why the study?
Long non-coding RNA MIAT has been identified as a risk factor for myocardial infarction, but its mechanism of action in MI was not determined.
May identify MIAT inhibition as a target to limit post-MI mitochondrial injury; leaves open translation to human therapy.
Long non-coding RNA MIAT (lncR-MIAT) has recently been identified as a risk factor for myocardial infarction (MI). 1 However, how lncR-MIAT controls MI remained yet to be determined. To shed light on this issue, we firstly detected the expression of lncR-MIAT using qRT-PCR and found a robust elevation (>5-fold) of lncR-MIAT level in heart of MI mice relative to sham-operated control counterparts (Supplementary Fig. S1a ). This upregulation of lncR-MIAT was diminished after injection of lentivirus carrying a shRNA of lncR-MIAT (Lv-shMIAT) to silence endogenous lncR-MIAT in myocardium. Similarly, 3-fold increase of lncR-MIAT was observed in cultured neonatal mouse ventricular cells (NMVCs) in response to hypoxic insult, which was effectively mitigated by siRNA (siMIAT; Supplementary Fig. S1b ) that effectively silenced endogenous lncR-MIAT in NMVCs (Supplementary Fig. S1c ).
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Bai et al. (2021) conducted a letter in Myocardial infarction. lncRNA MIAT knockdown (Lv-shMIAT) vs. Sham operation or negative control vector (Lv-NC / siNC) was evaluated on Cardiac contractile function (ejection fraction and fractional shortening) and apoptosis. In a mouse model of myocardial infarction, knockdown of lncRNA MIAT significantly restored impaired cardiac contractile function by preventing TSPO-mediated mitochondrial damage and apoptosis.
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