microRNA-99a Reduces Lipopolysaccharide-Induced Oxidative Injury by Activating Notch Pathway in H9c2 Cells.

Abstract:

:microRNA-99a (miR-99a) is recently recognized as a key regulator in various cancers and cardiovascular diseases. In the present study, we sought to investigate the effects of miR-99a in rat cardiomyocyte H9c2 cells against oxidative injury induced by lipopolysaccharide (LPS).MTT assay, reactive oxygen species (ROS) assay, flow cytometry and lactate dehydrogenase (LDH) assay were respectively used to explore viability, ROS levels, apoptosis, and cell death in H9c2 cells. Quantitative PCR (qRT-PCR) was performed to confirm the expression of miR-99a. Western blot was performed to determine the expression of Notch pathway factors.LPS could significantly suppress viability and increase cell death, apoptosis, and ROS level (P < 0.05). However, miR-99a could significantly increase the viability and decrease apoptosis and ROS level of H9c2 cells (P < 0.05). Overexpression of miR-99a could activate a Notch pathway and regulate the expression of B-cell CLL/lymphoma 2 (BCL2) and cleaved caspase 3.Our study found that overexpression of miR-99a could attenuate LPS-induced oxidative injury in H9c2 cells, possibly via a Notch pathway. These findings suggest that miR-99a may be a key factor in cardiomyocyte oxidative injury and could be a new therapeutic strategy for cardiovascular diseases.

journal_name

Int Heart J

authors

Jing R,Zhou Z,Kuang F,Huang L,Li C

doi

10.1536/ihj.16-261

subject

Has Abstract

pub_date

2017-05-31 00:00:00

pages

422-427

issue

3

eissn

1349-2365

issn

1349-3299

journal_volume

58

pub_type

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