Long non‑coding RNA H19 inhibition ameliorates oxygen‑glucose deprivation‑induced cell apoptosis and inflammatory cytokine expression by regulating the microRNA‑29b/SIRT1/PGC‑1α axis.

Abstract:

:As one of the earliest discovered long non‑coding (lnc)RNAs, lncRNA H19 imprinted maternally expressed transcript (H19) participates in regulating ischemic stroke. The present study aimed to investigate the combined roles of lncRNA H19, microRNA (miR)‑29b, silent mating‑type information regulation 2 homolog 1 (SIRT1) and peroxisome proliferator‑activated receptor‑g co‑activator‑1α (PGC‑1α) following ischemic stroke. lncRNA H19 expression levels in the middle cerebral artery occlusion (MCAO) mouse model and HT22 cells subjected to oxygen‑glucose deprivation (OGD) were detected via reverse transcription‑quantitative PCR (RT‑qPCR). H19 small interfering RNA was used to knockdown H19 expression. Following OGD treatment, MTT, flow cytometry, ELISA, RT‑qPCR and western blotting assays were performed to assess cell proliferation, cell apoptosis, inflammatory cytokine concentrations, and lncRNA H19, miR‑29b, SIRT1, PGC‑1α expression levels, respectively. In the present study, MCAO model mice and OGD‑treated cells displayed significantly increased lncRNA H19 expression levels compared with sham mice and control cells, respectively. lncRNA H19 knockdown ameliorated OGD‑induced cell apoptosis and increases in inflammatory cytokine concentrations. Furthermore, lncRNA H19 knockdown also attenuated OGD‑mediated downregulation of miR‑29b, SIRT1 and PGC‑1α expression levels. Collectively, the results of the present study demonstrated that lncRNA H19 knockdown ameliorated OGD‑induced cell apoptosis and increases in inflammatory cytokine concentrations by regulating miR‑29b, SIRT1 and PGC‑1α expression levels, which suggested the potential role of lncRNA H19 in ischemic stroke.

journal_name

Mol Med Rep

authors

Xu J,Wang C,Meng F,Xu P

doi

10.3892/mmr.2020.11770

subject

Has Abstract

pub_date

2021-02-01 00:00:00

issue

2

eissn

1791-2997

issn

1791-3004

pii

131

journal_volume

23

pub_type

杂志文章