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Life Sci. 2019 Jul 29:116705. doi: 10.1016/j.lfs.2019.116705. [Epub ahead of print]

LncRNA AK139128 promotes cardiomyocyte autophagy and apoptosis in myocardial hypoxia-reoxygenation injury.

Author information

1
Department of Cardiology, Hospital 903 of PLA, Hangzhou City, Zhejiang Province 310013, China.
2
Department of Emergency, Zhuji People's Hospital of Zhejiang Province, Zhuji City, Zhejiang Province 311800, China. Electronic address: zhaochufeng_zj@yeah.net.

Abstract

AIMS:

Long noncoding RNA (lncRNAs) participate in various biological processes in a number of cardiovascular diseases. Recently, a novel lncRNA AK139128 was found to be differentially expressed in myocardial ischemia-reperfusion injury (MIRI) tissue compared to normal myocardial tissues. Its pathological role in MIRI however, remains unknown.

MATERIALS AND METHODS:

The expression level of AK139128 was investigated by quantitative real-time polymerase chain reaction assays (qRT-PCR) in MIRI tissues and cardiomyocytes. The effects of AK139128 in cell autophagy and apoptosis were determined using TUNEL assay, immunofluorescence assay and western blotting. Bioinformatics analysis and luciferase reporter assay were performed to verify the target relationship between AK139128, miR-499 and FOXO4.

KEY FINDINGS:

Results show that AK139128 was significantly up-regulated in MIRI tissues and cardiomyocytes. Knockdown of AK139128 impressively alleviates cardiomyocyte autophagy and apoptosis. Bioinformatics analysis and luciferase reporter assay showed that miR-499 targeted both 3'UTR of AK139128 and FOXO4 mRNA. Further functional experiments showed that miR-499 inhibitor eliminates the effects of knockdown of AK139128 on apoptosis and autophagy.

SIGNIFICANCE:

Taken together, results from this study suggests that lncRNA AK139128 mediates autophagy and apoptosis in MIRI via targeting miR-499/FOXO4 axis, and modulating their levels may provide a new approach to improve MIRI outcomes.

KEYWORDS:

AK139128; Apoptosis; Autophagy; FOXO4; Long noncoding RNA; miR-499

PMID:
31369757
DOI:
10.1016/j.lfs.2019.116705

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