Authors
Ayaka Hamaguchi, Hayato Fukuda, Mizuki Watanabe, Koichi Fujiwara, Keijo Fukushima, John W Regan, Asuka Inoue, Satoshi Shuto, Hiromichi Fujino
Published in
Prostaglandins & other lipid mediators. Pages 107118. Nov 07, 2026. Epub Nov 07, 2026.
Abstract
Prostaglandin E2 (PGE2) signals through E-type prostanoid (EP) receptors, among which EP4 receptors couple to Gαs protein to induce cAMP formation and also to Gαi protein to induce phosphorylation of extracellular signal-regulated kinases (ERKs). Although PGE2 acts as a pro-inflammatory mediator during the early phase of inflammation, PGE2-activated EP4 receptor signaling has also been implicated in the resolution phase. Resolvin E-series (RvEs), including RvE1, RvE2, and RvE3, are specialized pro-resolving mediators that promote the resolution of inflammation. We previously reported that RvE1 and RvE2, but not RvE3, suppressed cyclooxygenase-2 expression and PGE2 production. Because our previous studies addressed PGE2 production, we herein examined their impact on PGE2-stimulated EP4 receptor-mediated signaling. RvE3, but not RvE1 or RvE2, enhanced PGE2-stimulated cAMP formation, accompanied by increased EP4 receptor-mediated Gαs protein activation. In contrast, RvE3 did not increase Gαi protein activation or phosphorylation of ERKs. Therefore, RvE3 appears to selectively enhance EP4 receptor/Gαs protein-mediated cAMP signaling. Taken together with our previous findings, the present results suggest that RvE3 regulates PGE2-related responses through a mechanism that is distinct from those of RvE1 and RvE2, which may collectively contribute to the resolution of inflammation.
PMID:
42998705
Bibliographic data and abstract were imported from PubMed on 08 Nov 2026.
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