Chitinase-3-like protein 1 ameliorates atherosclerotic responses via PPAR delta-mediated suppression of inflammation and ER stress
- Authors
- Jung, Tae Woo; Park, Hyung Sub; Choi, Geum Hee; Kim, Daehwan; Jeong, Ji Hoon; Lee, Taeseung
- Issue Date
- Aug-2018
- Publisher
- WILEY
- Keywords
- apoptosis; chitinase 3-like protein 1; HUVECs; inflammation; oxygen-regulated protein 150; peroxisome proliferator-activated receptor delta
- Citation
- JOURNAL OF CELLULAR BIOCHEMISTRY, v.119, no.8, pp 6795 - 6805
- Pages
- 11
- Journal Title
- JOURNAL OF CELLULAR BIOCHEMISTRY
- Volume
- 119
- Number
- 8
- Start Page
- 6795
- End Page
- 6805
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/1897
- DOI
- 10.1002/jcb.26873
- ISSN
- 0730-2312
1097-4644
- Abstract
- Chitinase 3-like protein 1 (CHI3L1) is a novel biomarker of systemic inflammation. However, the effects of CHI3L1 on the progression of atherosclerosis remain to be explored. In the current study, we found that CHI3L1 induces peroxisome proliferator-activated receptor delta (PPAR) expression, leading to a dose-dependent increase in oxygen-regulated protein 150 (ORP150) expression. We demonstrated that CHI3L1 suppresses atherosclerotic reactions caused by LPS treatment via a PPAR-dependent pathway. Treatment of HUVECs and THP-1 cells with CHI3L1 suppressed LPS-induced phosphorylation of nuclear factor kappa B (NFB) and secretion of proinflammatory cytokines such as TNF and MCP-1. In HUVECs, expression of adhesion molecules and LPS-stimulated adhesion of THP-1 cells to the endothelium were significantly reduced after CHI3L1 treatment. Furthermore, LPS-induced endoplasmic reticulum (ER) stress and cell apoptosis were significantly ameliorated after treatment of HUVECs with CHI3L1. Particularly, all of the pro-atherosclerotic effects were significantly mitigated by treatment with small interfering (si) RNA for PPAR. In conclusion, CHI3L1 ameliorates LPS-induced atherosclerotic reactions via PPAR-mediated suppression of inflammation and ER stress.
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