title: P2Y purinoceptors mediate ATP-induced changes in intracellular calcium and amylase release in acinar cells of mouse parotid glands.
abstract: Adenosine 5'-triphosphate (ATP) can act as an extracellular signal that regulates various cellular functions. The present study aimed to determine which purinoceptors play a role in ATP-induced changes in intracellular Ca(2+) ([Ca(2+)]i) and amylase secretion in mouse parotid glands. ATP induced a steep increase in [Ca(2+)]i in acinar cells. The removal of extracellular Ca(2+) or the use of Ca(2+) channel blockers slightly inhibited this increase. Inhibition of PLCγ by U73122 and of IP3 by xestospongin C did not completely block this increase. The purinoceptor antagonists suramin and reactive blue-2 strongly inhibited the ATP-induced changes in [Ca(2+)]i. 2-MeSATP induced a strong increase in [Ca(2+)]i, while Bz-ATP induced a small [Ca(2+)]i increase, and UTP and α,β-MeATP had no effect. The potency order of ATP analogs (2-MeSATP > ATP >> UTP) suggested that P2Y1 and P2Y12 play a significant role in the cellular response to ATP. RT-PCR revealed that P2X2,4,7 and P2Y1,2,10,12,14 were expressed in acinar cells. Ca(2+)-dependent exocytotic secretion of amylase was detected in parotid glands. These findings indicated that ATP activates P2Y receptors more than P2X receptors at low concentrations. Thus, P2Y receptors were found to be the main receptors involved in Ca(2+)-related cell homeostasis and amylase secretion in mouse parotid glands.
authors.affiliation: Department of Anatomy (Cell Biology), Iwate Medical University.
authors.forename: Kasumi
authors.initials: K
authors.lastname: Moriguchi-Mori
authors.forename: Hironori
authors.initials: H
authors.lastname: Higashio
authors.forename: Kanako
authors.initials: K
authors.lastname: Isobe
authors.forename: Miho
authors.initials: M
authors.lastname: Kumagai
authors.forename: Kana
authors.initials: K
authors.lastname: Sasaki
authors.forename: Yoh-ichi
authors.initials: Y
authors.lastname: Satoh
authors.forename: Akiyoshi
authors.initials: A
authors.lastname: Kuji
authors.forename: Tomoyuki
authors.initials: T
authors.lastname: Saino
mesh_terms: D061354:Acinar Cells / Q000187:drug effects / Q000378:metabolism*; D000255:Adenosine Triphosphate / Q000378:metabolism*; D000681:Amylases / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects; D004789:Enzyme Activation; D015870:Gene Expression; D042541:Intracellular Space / Q000378:metabolism; D051379:Mice; D010306:Parotid Gland / Q000166:cytology* / Q000378:metabolism*; D058912:Purinergic P2Y Receptor Agonists / Q000494:pharmacology; D058921:Purinergic P2Y Receptor Antagonists / Q000494:pharmacology; D012333:RNA, Messenger / Q000235:genetics; D058470:Receptors, Purinergic P2Y / Q000235:genetics / Q000378:metabolism*
chemical_list: D058912:Purinergic P2Y Receptor Agonists; D058921:Purinergic P2Y Receptor Antagonists; D012333:RNA, Messenger; D058470:Receptors, Purinergic P2Y; D000255:Adenosine Triphosphate; D000681:Amylases; D002118:Calcium