In:
Journal of Cardiovascular Pharmacology, Ovid Technologies (Wolters Kluwer Health), Vol. 76, No. 5 ( 2020-11), p. 533-539
Abstract:
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.
Type of Medium:
Online Resource
ISSN:
0160-2446
DOI:
10.1097/FJC.0000000000000906
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
2020
detail.hit.zdb_id:
2049700-3
SSG:
15,3
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