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LncRNA Gm4419 contributes to OGD/R injury of cerebral microglial cells via IκB phosphorylation and NF-κB activation.

Abstract：

:Ischemic stroke is one of major causes of adult morbidity. Recent studies have shown that over-activated microglial cells play a critical role in aggravating cerebral oxygen glucose deprivation/reoxygenation (OGD/R) damage by releasing excessive inflammatory cytokines. However, the involving mechanisms are not distinct yet. Long non-coding RNAs (lncRNAs) have been reported to in participate in lots of complicated biological processes. Our understandings of the relationship between lncRNAs and OGD/R injury are largely limited. In this study, we demonstrated that a lncRNA Gm4419 functioned as a crucial mediator in the activation of NF-κB signaling pathway, causing neuroinflammation damage during OGD/R. Gm4419 was abnormally up-regulated in OGD/R-treated microglial cells. We found that the high level of Gm4419 promoted the phosphorylation of IκBα by physically associating with IκBα, therefore, led to increased nucleus NF-κB levels for the transcriptional activation of TNF-α, IL-1β and IL-6. In addition, we also demonstrated that knockdown of Gm4419 functioned as NF-κB inhibitor in OGD/R microglial cells, showing that down-regulation of Gm4419 had protective role against OGD/R injury. In summary, Gm4419 is required for microglial cell OGD/R injury though the activation of NF-κB signaling. Thus, Gm4419 appears to be a promising therapeutic target for ischemic stroke.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Wen Y,Yu Y,Fu X

doi

10.1016/j.bbrc.2017.05.005

subject

Has Abstract

pub_date

2017-06-10 00:00:00

pages

923-929

issue

4

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(17)30851-3

journal_volume

487

pub_type

杂志文章

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