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LncRNA HOXA-AS2 represses endothelium inflammation by regulating the activity of NF-κB signaling.

Abstract：

BACKGROUND AND AIMS:Endothelium inflammation, which can lead to endothelial activation and dysfunction, is widely accepted as the major event in multiple vascular disorders. The lncRNA HOXA-AS2 was previously reported to be involved in multiple inflammation-linked cancers. However, the role of HOXA-AS2 in endothelium inflammation is poorly understood. This study aims to determine the regulatory role of HOXA-AS2 in endothelium inflammation and related vascular diseases. METHODS:High throughput mRNA sequencing was performed to establish expression profiles after HOXA-AS2 depletion. We extracted total RNAs of human peripheral blood mononuclear cells from normal control group and experimental group with carotid artery atherosclerosis, and performed qRT-PCR to assay the correlation between HOXA-AS2 expression and inflammatory vascular diseases. RESULTS:Inhibition of HOXA-AS2 can induce the activation of NF-κB signaling and subsequent inflammatory response. More importantly, HOXA-AS2 is inversely found to be inversely regulated by NF-κB in a negative feedback manner by helping recruit BRD4/P-TEFb complex to HOXA-AS2 promoter region, therefore facilitating release of the promoter-proximal paused RNA polymerase II and activating transcription elongation. CONCLUSIONS:We identify HOXA-AS2 as a critical repressor of endothelium inflammation. Moreover, this study offers us a new way to balance the NF-κB signaling-driven excessive endothelium inflammation by establishing a NF-κB/HOXA-AS2 negative feedback loop. Based on these findings, we conclude that HOXA-AS2 may serve as a crucial therapeutic target for various vascular disorders which are significantly associated with endothelium inflammation.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Zhu X,Liu Y,Yu J,Du J,Guo R,Feng Y,Zhong G,Jiang Y,Lin J

doi

10.1016/j.atherosclerosis.2018.12.012

subject

Has Abstract

pub_date

2019-02-01 00:00:00

pages

38-46

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(18)31543-0

journal_volume

281

pub_type

杂志文章

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