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• W2904687091 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." @default.
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• W2904687091 date "2019-02-01" @default.
• W2904687091 modified "2023-10-18" @default.
• W2904687091 title "LncRNA HOXA-AS2 represses endothelium inflammation by regulating the activity of NF-κB signaling" @default.
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• W2904687091 doi "https://doi.org/10.1016/j.atherosclerosis.2018.12.012" @default.
• W2904687091 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30658190" @default.
• W2904687091 hasPublicationYear "2019" @default.
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