beta-Arrestin 2 Mediates G Protein-Coupled Receptor 43 Signals to Nuclear Factor-kappa B
- Authors
- Lee, Su Ui; In, Hyun Ju; Kwon, Mi So; Park, Bi-oh; Jo, Mimi; Kim, Mun-Ock; Cho, Sungchan; Lee, Sangku; Lee, Hyun-Jun; Kwak, Young Shin; Kim, Sunhong
- Issue Date
- 11월-2013
- Publisher
- PHARMACEUTICAL SOC JAPAN
- Keywords
- G protein-coupled receptor 43; beta-arrestin; nuclear factor-kappa B; inflammation
- Citation
- BIOLOGICAL & PHARMACEUTICAL BULLETIN, v.36, no.11, pp.1754 - 1759
- Indexed
- SCIE
SCOPUS
- Journal Title
- BIOLOGICAL & PHARMACEUTICAL BULLETIN
- Volume
- 36
- Number
- 11
- Start Page
- 1754
- End Page
- 1759
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/101808
- ISSN
- 0918-6158
- Abstract
- G-protein coupled receptor 43 (GPR43) serves as a receptor for short-chain fatty acids (SCFAs), implicated in neutrophil migration and inflammatory cytokine production. However, the intracellular signaling pathway mediating GPR43 signaling remains unclear. Here, we show that beta-arrestin 2 mediates the internalization of GPR43 by agonist. Agonisrn of GPR43 reduced the phosphorylation and nuclear translocation of nuclear factor-kappa B (NF-kappa B), which was relieved by short interfering RNA (siRNA) of beta-arrestin 2. Subsequently, mRNA expression of proinflammatory cytokines, interleukin (IL)-6 and IL-1 beta, was downregulated by activation of GPR43 and knockdown of beta-arrestin 2 recovered the expression of the cytokines. Taken together, these results suggest that GPR43 may be a plausible target for a variety of inflammatory diseases.
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Collections - College of Pharmacy > Department of Pharmaceutical Science > 1. Journal Articles
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