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Resetting of peripheral circadian clock by prostaglandin E 2
Author(s) -
Tsuchiya Yoshiki,
Minami Itsunari,
Kadotani Hiroshi,
Nishida Eisuke
Publication year - 2005
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/sj.embor.7400356
Subject(s) - circadian rhythm , prostaglandin e2 receptor , suprachiasmatic nucleus , endocrinology , prostaglandin e , circadian clock , agonist , medicine , clock , receptor , biology , in vivo , hypothalamus , chemistry , microbiology and biotechnology
In mammals, the master circadian pacemaker is located in the suprachiasmatic nucleus (SCN) of the hypothalamus. The SCN is thought to drive peripheral oscillators by controlling neuronal and humoral signals that can entrain the peripheral clocks. Here, we show that prostaglandin E 2 (PGE 2 ), a proinflammatory compound known to have diverse biological effects, is able to act as an in vivo clock‐resetting agent. We find that in cultured NIH3T3 fibroblasts, PGE 2 is able to induce transient expression of Period 1 messenger RNA and the following circadian oscillation of clock gene expression. Furthermore, we demonstrate that intraperitoneal administration of PGE 2 results in the phase shift of circadian gene expression in mouse peripheral tissues in a time‐dependent manner. This phase shift is also induced by the EP1/EP3 agonist sulprostone but not by the EP2 agonist butaprost. The PGE 2 ‐induced phase shift is inhibited by the EP1 antagonist SC‐51322. These results suggest that PGE 2 acts as an in vivo clock‐resetting factor by means of the EP1 subtype of PGE receptors.