STAT1 regulates MD-2 expression in monocytes of sepsis via miR-30a.

Abstract:

:Sepsis is a major cause of morbidity and mortality in critically ill patients. MD-2 is a 25-kDa lipopolysaccharide (LPS)-binding protein that forms a heterodimer with TLR42, but its regulation in sepsis is not clear. This study aims to investigate the molecular mechanism of regulation of MD-2. Inflammation cytokines in monocytes were analyzed by real-time RT-PCR and ELISA, and it was found that IL-10 was elevated significantly in the monocytes with LPS treatment. And then, when the cells were treated with IL-10, STAT1 was activated in the monocytes using Western blotting. It was also found that STAT1 could enhance MD-2 expression on transcriptional and posttranscriptional levels. Finally, miR-30a was predicted to the molecule that may regulate STAT1 expression. It was verified that STAT1 was a new target gene of miR-30a. miR-30a could inhibit IL-10-induced cytokine release by targeting STAT1-MD-2 in monocytes. In conclusion, this study for the first time demonstrated that miR-30a inhibits MD-2 expression by targeting of STAT1 in human monocytes.

journal_name

Inflammation

journal_title

Inflammation

authors

Wang Y,Li T,Wu B,Liu H,Luo J,Feng D,Shi Y

doi

10.1007/s10753-014-9922-1

subject

Has Abstract

pub_date

2014-12-01 00:00:00

pages

1903-11

issue

6

eissn

0360-3997

issn

1573-2576

journal_volume

37

pub_type

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