β-Arrestin 2 Mediates G Protein-Coupled Receptor 43 Signals to Nuclear Factor-κB

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 β-arrestin 2 mediates th...

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Bibliographic Details
Published in:Biological & pharmaceutical bulletin 2013/11/01, Vol.36(11), pp.1754-1759
Main Authors: Lee, Su Ui, In, Hyun Ju, Kwon, Mi So, Park, Bi-oh, Jo, Minmi, Kim, Mun-Ock, Cho, Sungchan, Lee, Sangku, Lee, Hyun-Jun, Kwak, Young Shin, Kim, Sunhong
Format: Article
Language:English
Subjects:
Arrestins - metabolism
beta-Arrestin 2
beta-Arrestins
G protein-coupled receptor 43
HEK293 Cells
HeLa Cells
Humans
inflammation
NF-kappa B - metabolism
nuclear factor-κB
Receptors, Cell Surface - metabolism
β-arrestin
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Summary: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 β-arrestin 2 mediates the internalization of GPR43 by agonist. Agonism of GPR43 reduced the phosphorylation and nuclear translocation of nuclear factor-κB (NF-κB), which was relieved by short interfering RNA (siRNA) of β-arrestin 2. Subsequently, mRNA expression of proinflammatory cytokines, interleukin (IL)-6 and IL-1β, was downregulated by activation of GPR43 and knockdown of β-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.
ISSN:0918-6158
1347-5215
DOI:10.1248/bpb.b13-00312