Impact of Long Non-Coding RNA Metastasis-Associated Lung Adenocarcinoma Transcript 1 on the Susceptibility of High Glucose-Treated Cardiomyocytes to Hypoxia/Reoxygenation

To estimate the effect of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) on susceptibility of high glucose (HG)-treated cardiomyocytes (CMs) to hypoxia/reoxygenation (H/R). Forty healthy rats were assigned to the control, diabetes mellitus (DM), DM + ischemia/reperfusion injury (IRI) control, and DM IRI groups (n = 10 for each group). Rat CMs (H9C2) were subjected to HG and H/R treatments. LncRNA MALAT1 and cyclic-AMP responsive element modulator (CREM) mRNA levels were measured using quantitative polymerase chain reaction, and protein levels of CREM, myeloid differentiation primary response protein 88 (MyD88), interleukin-1 receptor-associated kinase 1 (IRAK1), tumor necrosis factor receptor associated factor 6 (TRAF6), tumor necrosis factor-a (TNF-a), and interleukin-6 (IL-6) were quantified using western blotting. Flow cytometry was applied for detection of apoptosis, and a cell viability analyzer determined the number of living cells.IRI induced myocardial apoptosis and elevated lncRNA MALAT1, CREM, and MyD88/IRAK1/TRAF6 levels in DM group mice.In H9C2 cells, HG treatment downIP: 182.75.148.10 On: Sat, 20 Aug 2022 10:36:38 regulated CREM expression, which resulted in the downregulation of lncRNA MALAT1 expression, reducing the susceptibility to H/R, increasing cell viability and apoptosis, decreasing the activity of the MyD88/IRAK1/TRAF6 signaling pathway, and suppressing TNF-a and IL-6 expression. LncRNA MALAT1 regulates the susceptibility of HG-treated CMs to H/R through the MyD88 signaling pathway.