Hypoxia-Induced Myocardial Cell Injury

TUG1[LncRNA]

miR-29a-3p[miRNA]

NA[mRNA]

AC16 Cells

Homo sapiens (human)

J Cardiovasc Pharmacol. 2020 Nov;76(5):533-539. doi: 10.1097/FJC.0000000000000906.

LncRNA TUG1 Contributes to Hypoxia-Induced Myocardial Cell Injury Through Downregulating miR-29a-3p in AC16 Cells.

Dual-luciferase reporter assay;Western blot;Flow Cytometry assay;Luciferase reporter assay;

Myocardial ischemia is a common reason that causes human death globally. Long noncoding RNA taurine upregulated 1 (TUG1) serves as an oncogene in a variety of cancers. In this article, we aimed to investigate the role of TUG1 and its underlying signal pathway in hypoxia-induced myocardial cell injury. Cell viability, apoptosis, and lactate dehydrogenase (LDH) release were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, flow cytometry, western blot assay, and LDH cytotoxicity assay. Quantitative real-time polymerase chain reaction was applied to measure the enrichment of TUG1 and miR-29a-3p. MiR-29a-3p was predicted as a target of TUG1 by StarBase bioinformatic software, and the target relationship between TUG1 and miR-29a-3p was verified by dual-luciferase reporter assay. Hypoxia treatment induced the apoptosis and LDH release while inhibited the viability of AC16 cells. TUG1 was markedly upregulated while the level of miR-29a-3p was notably decreased in hypoxia-stimulated AC16 cells. TUG1 contributed to hypoxia-induced AC16 injury. MiR-29a-3p depletion intensified hypoxia-induced AC16 damage. TUG1 negatively regulated the expression of miR-29a-3p through their direct interaction in AC16 cells. TUG1 silencing-mediated influences in hypoxia-induced AC16 cells were partly reversed by the interference of miR-29a-3p. In conclusion, TUG1 accelerated hypoxia-induced AC16 injury through inversely modulating the level of miR-29a-3p. TUG1/miR-29a-3p axis might be an underlying therapeutic target for myocardial ischemia.