title: Inorganic polyphosphate in human osteoblast-like cells.
abstract: Significant amounts of inorganic polyphosphates and of polyphosphate-degrading exopolyphosphatase activity were detected in human mandibular-derived osteoblast-like cells. The amount of both soluble and insoluble long-chain polyphosphate in unstimulated osteoblast-like cells was higher than in human gingival cells, erythrocytes, peripheral blood mononuclear cells, and human blood plasma. The cellular content of polyphosphate in osteoblast-like cells strongly decreased after a combined treatment of the cells with the stimulators of osteoblast proliferation and differentiation, dexamethasone, beta-glycerophosphate, epidermal growth factor, and ascorbic acid. The amount of soluble long-chain polyphosphate, but not the amount of insoluble long-chain polyphosphate, further decreased after an additional treatment with 1alpha,25-dihydroxyvitamin D3 (1,25(OH)2D3). The decrease in polyphosphate content during treatment with dexamethasone, beta-glycerophosphate, epidermal growth factor, and ascorbic acid was accompanied by a decrease in exopolyphosphatase, pyrophosphatase, and alkaline phosphatase activity. However, additional treatment with 1,25(OH)2D3 resulted in an increase in these enzyme activities. Osteoblast-like cell exopolyphosphatase activity and exopolyphosphatase activity in yeast, rat tissues, and human leukemia cell line HL60 were inhibited by the bisphosphonates etidronate and, to a lesser extent, clodronate and pamidronate. From our results, we assume that inorganic polyphosphate may be involved in modulation of the mineralization process in bone tissue.
authors.affiliation: Poliklinik für Zahnerhaltung und Parodontologie, Medizinische Hochschule, Hannover, Germany.
authors.forename: G
authors.initials: G
authors.lastname: Leyhausen
authors.forename: B
authors.initials: B
authors.lastname: Lorenz
authors.forename: H
authors.initials: H
authors.lastname: Zhu
authors.forename: W
authors.initials: W
authors.lastname: Geurtsen
authors.forename: R
authors.initials: R
authors.lastname: Bohnensack
authors.forename: W E
authors.initials: WE
authors.lastname: Müller
authors.forename: H C
authors.initials: HC
authors.lastname: Schröder
mesh_terms: D017766:Acid Anhydride Hydrolases / Q000378:metabolism; D000469:Alkaline Phosphatase / Q000378:metabolism; D000818:Animals; D002117:Calcitriol / Q000494:pharmacology; D002454:Cell Differentiation / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects; D002478:Cells, Cultured; D003907:Dexamethasone / Q000494:pharmacology; D004164:Diphosphonates / Q000494:pharmacology; D004815:Epidermal Growth Factor / Q000494:pharmacology; D012968:Etidronic Acid / Q000494:pharmacology; D005994:Glycerophosphates / Q000494:pharmacology; D018922:HL-60 Cells; D006801:Humans; D043564:Inorganic Pyrophosphatase; D008334:Mandible / Q000166:cytology / Q000378:metabolism; D010006:Osteoblasts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D011122:Polyphosphates / Q000378:metabolism*; D011755:Pyrophosphatases / Q000378:metabolism; D051381:Rats; D012995:Solubility
chemical_list: D004164:Diphosphonates; D005994:Glycerophosphates; D011122:Polyphosphates; D004815:Epidermal Growth Factor; D003907:Dexamethasone; D000469:Alkaline Phosphatase; D017766:Acid Anhydride Hydrolases; D011755:Pyrophosphatases; D043564:Inorganic Pyrophosphatase; C020137:exopolyphosphatase; D002117:Calcitriol; D012968:Etidronic Acid; C031463:beta-glycerophosphoric acid