NEAT1 promotes myocardial ischemia‐reperfusion injury via activating the MAPK signaling pathway

Xian‐Jin Du; Jie Wei; Dan Tian; Chen Yan; Peng Hu; Xu Wu; Wenbin Yang; Xiaorong Hu

doi:10.1002/jcp.28516

journal article Apr 04, 2019

NEAT1 promotes myocardial ischemia‐reperfusion injury via activating the MAPK signaling pathway

Xian‐Jin Du

Wenbin Yang Xiaorong Hu

Journal of Cellular Physiology Vol. 234 No. 10 pp. 18773-18780 · Wiley

View at Publisher Save 10.1002/jcp.28516

Abstract

AbstractMyocardial ischemia‐reperfusion (IR) injury is a common cardiovascular problem, which remains a major cause of death in the world. Emerging evidence has suggested that long noncoding RNAs are crucial players in myocardial injury. However, the functional involvement of nuclear enriched abundant transcript 1 (NEAT1) in myocardial IR injury remains poorly investigated. Our study focused on the mechanism of NEAT1 in myocardial IR injury. Here, we reported a crucial role for NEAT1 in exacerbating cardiac IR injury. NEAT1 was greatly increased in myocardial IR injury mice models. As exhibited knockdown of NEAT1 resulted in attenuated myocardial IR injury in vivo. In addition, we found that NEAT1 was dramatically induced by hypoxia/reoxygenation in H9c2 cells. Lactate dehydrogenase (LDH), malondialdehyde, reactive oxygen species levels, and endoplasmic reticulum stress‐regulated cardiomyocyte apoptosis were inhibited by the downregulation of NEAT1. Here, it was shown that knockdown of NEAT1 was able to repress tumor necrosis factor‐α, interleukin‐1β, and IL‐6 expression. The silence of NEAT1 protected against IR injury via decreasing troponin levels, cardiocytes apoptosis, creatine kinase, and lactate LDH release in vivo. Meanwhile, the mitogen‐activated protein kinase (MAPK) signaling was involved in NEAT1‐mediated myocardial IR injury. In summary, our data indicated that NEAT1 contributed to myocardial IR injury via activating the MAPK pathway.

Topics

No keywords indexed for this article. Browse by subject →

References

32

[1]

10.3390/ijms161023651

[2]

10.1161/circulationaha.109.880187

[3]

10.1007/s10528-007-9137-3

[4]

10.3389/fcvm.2018.00073

[5]

10.1098/rsob.170121

[6]

The GENCODE v7 catalog of human long noncoding RNAs: Analysis of their gene structure, evolution, and expression

Thomas Derrien, Rory Johnson, Giovanni Bussotti et al.

Genome Research 10.1101/gr.132159.111

[7]

10.3389/fgene.2018.00471

[8]

10.2459/jcm.0b013e32836499cd

[9]

Jiang M. "Role of spinal MAPK‐ERK signal pathway in myocardial IR injury" Chinese Journal of Contemporary Pediatrics (2013)

[10]

10.1016/j.addr.2015.05.012

[11]

10.1002/1878-0261.12404

[12]

10.3109/13880209.2015.1014569

[13]

10.1016/j.ijbiomac.2017.07.053

[14]

10.1159/000374006

[15]

10.1016/j.atherosclerosis.2018.08.031

[16]

10.1161/01.cir.99.13.1685

[17]

10.1016/s0167-5273(96)02854-9

[18]

10.1016/s1053-2498(03)00102-5

[19]

10.1080/14728222.2018.1439015

[20]

10.1096/fj.02-0729fje

[21]

10.1016/j.cell.2009.02.006

[22]

10.1097/fjc.0b013e318279b7b1

[23]

Mechanisms of Myocardial ischemia–reperfusion Injury and the Cytoprotective Role of Minocycline: Scope and Limitations

Guramrinder S Thind, Pratik R Agrawal, Benjamin Hirsh et al.

Future Cardiology 10.2217/fca.14.76

[24]

10.1146/annurev.physiol.010908.163111

[25]

Xiong J. "Cholinergic anti‐inflammatory pathway: A possible approach to protect against myocardial ischemia reperfusion injury" Chinese Medical Journal (2010)

[26]

10.18632/oncotarget.13737

[27]

10.3892/etm.2016.3777

[28]

10.1016/j.hlc.2017.09.011

[29]

10.1186/1471-2261-13-39

[30]

10.1590/1414-431x20186555

[31]

10.3892/etm.2017.4653

[32]

10.1016/j.cardiores.2006.02.025

Metrics

40

Citations

32

References

Details

Published: Apr 04, 2019
Vol/Issue: 234(10)
Pages: 18773-18780
License: View

Authors

X

Xian‐Jin Du