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- Title
Lipocalin-type prostaglandin D synthase regulates light-induced phase advance of the central circadian rhythm in mice.
- Authors
Kawaguchi, Chihiro; Shintani, Norihito; Hayata-Takano, Atsuko; Hatanaka, Michiyoshi; Kuromi, Ai; Nakamura, Reiko; Yamano, Yui; Shintani, Yusuke; Nagai, Katsuya; Tsuchiya, Soken; Sugimoto, Yukihiko; Ichikawa, Atsushi; Okuno, Yasushi; Urade, Yoshihiro; Hirai, Hiroyuki; Nagata, Kin-ya; Nakamura, Masataka; Narumiya, Shuh; Nakazawa, Takanobu; Kasai, Atsushi
- Abstract
We previously showed that mice lacking pituitary adenylate cyclase-activating polypeptide (PACAP) exhibit attenuated light-induced phase shift. To explore the underlying mechanisms, we performed gene expression analysis of laser capture microdissected suprachiasmatic nuclei (SCNs) and found that lipocalin-type prostaglandin (PG) D synthase (L-PGDS) is involved in the impaired response to light stimulation in the late subjective night in PACAP-deficient mice. L-PGDS-deficient mice also showed impaired light-induced phase advance, but normal phase delay and nonvisual light responses. Then, we examined the receptors involved in the response and observed that mice deficient for type 2 PGD2 receptor DP2/CRTH2 (chemoattractant receptor homologous molecule expressed on Th2 cells) show impaired light-induced phase advance. Concordant results were observed using the selective DP2/CRTH2 antagonist CAY10471. These results indicate that L-PGDS is involved in a mechanism of light-induced phase advance via DP2/CRTH2 signaling. Kawaguchi et al. show that mice deficient in lipocalin-type prostaglandin (PG) D synthase (L-PGDS) exhibit impaired light-induced phase advance, but normal phase delay and nonvisual light responses. This study suggests the role of L-PGDS for the light-induced phase advance possibly via a chemoattractant receptor DP2/CRTH2.
- Subjects
PROSTAGLANDINS; SYNTHASES; CIRCADIAN rhythms; RAT physiology; LIPOCALIN-1
- Publication
Communications Biology, 2020, Vol 3, Issue 1, pN.PAG
- ISSN
2399-3642
- Publication type
Article
- DOI
10.1038/s42003-020-01281-w