Regulation of CREB phosphorylation by cAMP and Ca2+ in parotid acinar cells.
Since various secretory stimuli regulate not only secretion but also protein, RNA, and DNA syntheses in salivary glands, we evaluated the effect of secretory stimuli on the phosphorylation state of CREB (cAMP response element-binding protein). Isoproterenol, forskolin, and CPS-cAMP markedly stimulated the phosphorylation of CREB in parotid acinar cells, and PKA inhibitors H-8 and H-89 dose-dependently inhibited it. In contrast, carbachol (CCH) and A23187 decreased CREB phosphorylation, but CCH did not decrease it in the absence of extracellular Ca2+. Although protein phosphatase inhibitor calyculin A alone markedly increased the phosphorylation, it could not prevent CCH-induced dephosphorylation of CREB. CaM kinase IV, a putative protein kinase for CREB in response to Ca2+ elevation, was undetectable in parotid acinar cells.
Takuma
T
T
Department of Oral Biochemistry, School of Dentistry, Health Sciences University of Hokkaido, Tobetsu, Japan. takuma@hucc.hokudai.ac.jp
Tajima
Y
Y
Ichida
T
T
D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D000900:Anti-Bacterial Agents / Q000494:pharmacology; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002217:Carbachol / Q000494:pharmacology; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism*; D017362:Cyclic AMP Response Element-Binding Protein / Q000187:drug effects* / Q000378:metabolism; D015151:Immunoblotting; D007545:Isoproterenol / Q000494:pharmacology; D018721:Muscarinic Agonists / Q000494:pharmacology; D010306:Parotid Gland / Q000187:drug effects* / Q000378:metabolism; D010766:Phosphorylation / Q000187:drug effects; D051381:Rats
D000318:Adrenergic beta-Agonists; D000900:Anti-Bacterial Agents; D017362:Cyclic AMP Response Element-Binding Protein; D018721:Muscarinic Agonists; D005576:Colforsin; D000001:Calcimycin; D002217:Carbachol; D000242:Cyclic AMP; D007545:Isoproterenol; D002118:Calcium