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Gq/11‐induced intracellular calcium mobilization mediates Per2 acute induction in Rat‐1 fibroblasts
Author(s) -
Takashima Naoyuki,
Fujioka Atsuko,
Hayasaka Naoto,
Matsuo Ayako,
Takasaki Jun,
Shigeyoshi Yasufumi
Publication year - 2006
Publication title -
genes to cells
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.912
H-Index - 115
eISSN - 1365-2443
pISSN - 1356-9597
DOI - 10.1111/j.1365-2443.2006.00999.x
Subject(s) - biology , mobilization , intracellular , calcium in biology , microbiology and biotechnology , calcium , medicine , history , archaeology
Phase resetting is one of the essential properties of circadian clocks that is required for the adjustment to a particular environment and the induction of Per1 and Per2 clock genes is believed to be a primary molecular event during this process. Although the intracellular signal transduction pathway underlying Per1 gene activation has been well characterized, the mechanisms that control Per2 up‐regulation have not yet been elucidated. In our present study, we demonstrate that Gq/11 coupled receptors mediate serum‐induced immediate rat Per2 (r Per2 ) transactivation in Rat‐1 fibroblasts via intracellular Ca 2+ mobilization. Stimulation of these cells with a high concentration of serum was found to rapidly increase the intracellular Ca 2+ levels and strongly up‐regulated r Per2 gene. r Per2 induction by serum stimulation was abrogated by intracellular Ca 2+ chelation and depletion of intracellular Ca 2+ store, which suggests that the calcium mobilization is necessary for the up‐regulation of r Per2 gene. In addition, suppression of Gq/11 function was observed to inhibit both Ca 2+ mobilization and r Per2 induction. Further, we demonstrated that endothelin‐induced acute r Per2 transactivation via Gq/11‐coupled endothelin receptors is also suppressed by a Gq/11 specific inhibitor. These findings together suggest that serum and endothelin utilize a common Gq/11‐PLC mediated pathway for the transactivation of r Per2 , which involves the mobilization of calcium from the intracellular calcium store.