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2016 ; 13
(1
): 98-108
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Long non-coding RNA ANRIL regulates inflammatory responses as a novel component
of NF-?B pathway
#MMPMID26618242
Zhou X
; Han X
; Wittfeldt A
; Sun J
; Liu C
; Wang X
; Gan LM
; Cao H
; Liang Z
RNA Biol
2016[]; 13
(1
): 98-108
PMID26618242
show ga
Antisense Noncoding RNA in the INK4 Locus (ANRIL) is the prime candidate gene at
Chr9p21, the well-defined genetic risk locus associated with multiple human
diseases including coronary artery disease (CAD), while little is known regarding
its role in the pathological processes. Endothelial dysfunction triggers
atherosclerotic processes that are causatively linked to CAD. To evaluate the
function of ANRIL in human endothelial cells (ECs), we examined ANRIL expression
under pathological stimuli and found ANRIL was markedly induced by
pro-inflammatory factors. Loss-of-function and chromatin immunoprecipitation
approaches revealed that NF-?B mediates TNF-? induced ANRIL expression. RNA
sequencing revealed that ANRIL silencing dysregulated expression of inflammatory
genes including IL6 and IL8 under TNF-? treatment. We explored the regulatory
mechanism of ANRIL on IL6/8 and found that Yin Yang 1 (YY1), an ANRIL binding
transcriptional factor revealed by RNA immunoprecipitation, was required for
IL6/8 expression under TNF-? treatment. YY1 was enriched at promoter loci of
IL6/8 and ANRIL silencing impaired the enrichment, indicating a cooperation
between ANRIL and YY1 in the regulation of inflammatory genes. For the first
time, we establish the connection between ANRIL and NF-?B pathway and show that
ANRIL regulates inflammatory responses through binding with YY1. The newly
identified TNF-?-NF-?B-ANRIL/YY1-IL6/8 pathway enhances understanding of the
etiology of CAD and provides potential therapeutic target for treatment of CAD.
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