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Apolipoprotein CIII regulates lipoprotein-associated phospholipase A2 expression via the MAPK and NFκB pathways.

Authors
  • Han, Xiaolei
  • Wang, Tiedong
  • Zhang, Jifeng
  • Liu, Xingxing
  • Li, Zhuang
  • Wang, Gangqi
  • Song, Qi
  • Pang, Daxin
  • Ouyang, Hongsheng
  • Tang, Xiaochun
Type
Published Article
Journal
Biology open
Publication Date
Jan 01, 2015
Volume
4
Issue
5
Pages
661–665
Identifiers
DOI: 10.1242/bio.201410900
PMID: 25836672
Source
Medline
Keywords
License
Unknown

Abstract

Apolipoprotein CIII (apo CIII), a small glycoprotein that binds to the surfaces of certain lipoproteins, is associated with inflammatory and atherogenic responses in vascular cells. Lipoprotein-associated phospholipase A2 (Lp-PLA2) has been proposed as an inflammatory biomarker and potential therapeutic target for cardiovascular disease (CVD). Here, we report that apo CIII increases Lp-PLA2 mRNA and protein levels in dose- and time- dependent manner in human monocytic THP-1 cells, and the increase can be abolished by MAPK and NFκB pathway inhibitors. Lp-PLA2 inhibitor, 1-linoleoyl glycerol attenuates the inflammation induced by apo CIII. In turn, exogenous Lp-PLA2 expression upregulates apo CIII and the upregulation can be inhibited by 1-linoleoyl glycerol in HepG2 cells. Moreover, plasma Lp-PLA2 level is correlated with apo CIII expression in pig liver. In vivo, Lp-PLA2 expression in monocytes and its activity in serum were significantly increased in human apo CIII transgenic porcine models compared with wild-type pigs. Our results suggest that Lp-PLA2 and apo CIII expression level is correlated with each other in vitro and in vivo.

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