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Nuclear IL-33 is a transcriptional regulator of NF-κB p65 and induces endothelial cell activation.

Abstract：

:Interleukin (IL)-33, an IL-1 family member, acts as an extracellular cytokine by binding its cognate receptor, ST2. IL-33 is also a chromatin-binding transcriptional regulator highly expressed in the nuclei of endothelial cells. However, the function of IL-33 as a nuclear factor is poorly defined. Here, we show that IL-33 is a novel transcriptional regulator of the p65 subunit of the NF-κB complex and is involved in endothelial cell activation. Quantitative reverse transcriptase PCR and Western blot analyses indicated that IL-33 mediates the expression of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in endothelial cells basally and in response to tumor necrosis factor-a-treatment. IL-33-induced ICAM-1/VCAM-1 expression was dependent on the regulatory effect of IL-33 on the nuclear factor (NF)-κB pathway; NF-κB p65 expression was enhanced by IL-33 overexpression and, conversely, reduced by IL-33 knockdown. Moreover, NF-κB p65 promoter activity and chromatin immunoprecipitation analysis revealed that IL-33 binds to the p65 promoter region in the nucleus. Our data provide the first evidence that IL-33 in the nucleus of endothelial cells participates in inflammatory reactions as a transcriptional regulator of NF-κB p65.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Choi YS,Park JA,Kim J,Rho SS,Park H,Kim YM,Kwon YG

doi

10.1016/j.bbrc.2012.04.005

subject

Has Abstract

pub_date

2012-05-04 00:00:00

pages

305-11

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(12)00639-0

journal_volume

421

pub_type

杂志文章

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