title: Effects of bradykinin on Ca2+ mobilization and prostaglandin E2 release in human periodontal ligament cells.
abstract: In fura-2-loaded human periodontal ligament (HPDL) cells, bradykinin induced a rapidly transient increase and subsequently sustained increase in cytosolic Ca2+ ([Ca2+]i). When external Ca2+ was chelated by EGTA, the transient peak of [Ca2+]i was reduced and the sustained level was abolished, implying the Ca2+ mobilization consists of intracellular Ca2+ release and Ca2+ influx. Thapsigargin, a specific Ca(2+)-ATPase inhibitor for inositol 1,4,5-trisphosphate (1,4,5-IP3)-sensitive Ca2+ pool, induced an increased in [Ca2+]i in the absence of external Ca2+. After depletion of the intracellular Ca2+ pool by thapsigargin, the increase in [Ca2+]i induced by bradykinin was obviously reduced. Bradykinin also stimulated formation of inositol polyphosphates including 1,4,5-IP3. These results suggest that bradykinin stimulates intracellular Ca2+ release from the 1,4,5-IP3-sensitive Ca2+ pool. Bradykinin stimulated prostaglandin E2 (PGE2) release in the presence of external Ca2+, but not in the absence of external Ca2+. Ca2+ ionophore A23187 and thapsigargin evoked the release of PGE2 in the presence of external Ca2+ despite no activation of bradykinin receptors. These results indicate that bradykinin induces Ca2+ mobilization via activation of phospholipase C and PGE2 release caused by the Ca2+ influx in HPDL cells.
authors.affiliation: Department of Periodontology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Ogata
authors.forename: N
authors.initials: N
authors.lastname: Niisato
authors.forename: T
authors.initials: T
authors.lastname: Negishi
authors.forename: T
authors.initials: T
authors.lastname: Sakurai
authors.forename: S
authors.initials: S
authors.lastname: Furuyama
authors.forename: H
authors.initials: H
authors.lastname: Sugiya
mesh_terms: D009597:4-Nitrophenylphosphatase / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000096:biosynthesis; D000818:Animals; D001920:Bradykinin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D002614:Chelating Agents; D015232:Dinoprostone / Q000378:metabolism*; D004533:Egtazic Acid / Q000494:pharmacology; D005456:Fluorescent Dyes; D016257:Fura-2 / Q000031:analogs & derivatives; D015870:Gene Expression; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D007295:Inositol Phosphates / Q000378:metabolism*; D007700:Kinetics; D008022:Ligaments / Q000187:drug effects / Q000378:metabolism*; D015675:Osteocalcin / Q000096:biosynthesis; D010519:Periodontium / Q000187:drug effects / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis / Q000096:biosynthesis; D051381:Rats; D013997:Time Factors
chemical_list: D002614:Chelating Agents; D005456:Fluorescent Dyes; D007295:Inositol Phosphates; D012333:RNA, Messenger; D015675:Osteocalcin; C049925:fura-2-am; D004533:Egtazic Acid; D015544:Inositol 1,4,5-Trisphosphate; D000469:Alkaline Phosphatase; D009597:4-Nitrophenylphosphatase; D015232:Dinoprostone; D001920:Bradykinin; D002118:Calcium; D016257:Fura-2