GPR40 Agonism Modulates Inflammatory Reactions in Vascular Endothelial Cellsopen access
- Authors
- Kim, Joo Won; Roh, Eun; Choi, Kyung Mook; Yoo, Hye Jin; Hwang, Hwan-Jin; Baik, Sei Hyun
- Issue Date
- May-2022
- Publisher
- KOREAN DIABETES ASSOC
- Keywords
- Cell adhesion molecules; Human umbilical vein endothelial cells; Inflammation; Receptors; G-protein-coupled 40
- Citation
- DIABETES & METABOLISM JOURNAL, v.46, no.3, pp.506 - 511
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- DIABETES & METABOLISM JOURNAL
- Volume
- 46
- Number
- 3
- Start Page
- 506
- End Page
- 511
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/143420
- DOI
- 10.4093/dmj.2021.0092
- ISSN
- 2233-6079
- Abstract
- Endothelial dysfunction is strongly linked with inflammatory responses, which can impact cardiovascular disease. Recently, G protein-coupled receptor 40 (GPR40) has been investigated as a modulator of metabolic stress; however, the function of GPR40 in vascular endothelial cells has not been reported. We analyzed whether treatment of GPR40-specific agonists modulated the inflammatory responses in human umbilical vein endothelial cells (HUVECs). Treatment with LY2922470, a GPR40 agonist, significantly reduced lipopolysaccharide (LPS)-mediated nuclear factor-kappa B (NF-KB) phosphorylation and movement into the nucleus from the cytosol. However, treatment with another GPR40 agonist, TAK875, did not inhibit LPS-induced NF-KB activation. LPS treatment induced expression of adhesion molecules vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) and attachment of THP-1 cells to HUVECs, which were all decreased by LY2922470 but not TAK875. Our results showed that ligand-dependent agonism of GPR40 is a promising therapeutic target for overcoming inflammatory reactions in the endothelium.
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Collections - College of Medicine > Department of Medical Science > 1. Journal Articles
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