Incadronate and Etidronate Accelerate Phosphate-Primed Mineralization of MC4 Cells via ERK1/2-Cbfa1 Signaling Pathway in a Ras-Independent Manner: Further Involvement of Mevalonate-Pathway Blockade for Incadronate
スポンサーリンク
概要
- 論文の詳細を見る
Two types of bisphosphonates (BPs), incadronate (INC) and etidronate (ETI) accelerated phosphate (Pi)-primed mineralization of MC4 cells in a subnanomolar dose range. Intracellular signaling pathways involved were examined. 1) The effect of INC but not ETI was partially suppressed by two mevalonate (MVA) pathway metabolites, farnesylpyrophosphate (FPP) and geranylgeranylpyrophosphate (GGPP). 2) The BP-like accelerating effect was produced by statins and also by Toxin B, a Rho GTPases-specific inhibitor. 3) INC induced Cbfa1-nuclear localization within hours; and in an in vivo experiment using ovariectomized mice, its 3 weeks dosing exhibited the same effect in tibial extracts. 4) BPs promoted luciferase expression in murine p1.3-osteocalcin gene 2-luc and p6-osteoblast specific element 2-luc transfected cells, just as MVA, FPP and GGPP did independently and additively to INC. 5) BPs activated extracellular signal-regulated kinase (ERK1/2) in a Ras-independent manner within 5 min, and Pi was found to sensitize MC4 cells to BPs. MVA and its metabolites also activated ERKs but in a Ras-dependent manner and additively to INC. Ras dependency was determined using N17Ras-transfected cells. A MEK (MAP kinase-ERK kinase)-specific inhibitor PD98059 alone partly and with FPP completely blocked INC-induced mineralization. The results suggest that BPs act on Pi-sensitized MC4 cells to accelerate mineralization via nonRas-MEK-ERK1/2-Cbfa1 transactivation pathway and INC additionally acts by inhibiting the MVA pathway.
- 社団法人 日本薬理学会の論文
- 2001-05-01
著者
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Fujita Takashi
Department Of Cardiology Kanazawa University
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NAKAMUTA HIROMICHI
Department of Parmacology, Setsunan University
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KOIDA MASAO
Department of Parmacology, Setsunan University
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Fujita T
Division Of Oral Cytology And Cell Biology Department Of Developmental And Reconstructive Medicine N
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FUJITA Takuya
Ritsumeikan University College of Information Science and Engeneering
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FUKUYAMA Ryo
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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IZUMO Nobuo
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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MEGURO Toru
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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YASUTOMI Chigusa
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Setsunan University
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Fujita T
Ritsumeikan University College Of Information Science And Engeneering
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Izumo Nobuo
Department Of Pharmacology Daiichi College Of Pharmaceutical Sciences
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Meguro Toru
Department Of Pharmacology Faculty Of Pharmaceutical Sciences Setsunan University
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Meguro Toru
Department Of Pathology Yamagata University School Of Medicine
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Koida M
Department Of Pharmacology Faculty Of Pharmaceutical Sciences Setsunan University
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Koida Masao
Department Of Parmacology Setsunan University
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Fukuyama Tohru
Department Of Pharmacology Hiroshima International University
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Fukushima Tohru
Department Of Pharmacology Faculty Of Pharmaceutical Sciences Setsunan University
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Nakamuta H
Department Of Pharmacology Hiroshima International University
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Nakamuta Hiromichi
Department Of Parmacology Setsunan University
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Fujita Takashi
Department Of Breast Oncology Aichi Cancer Center Hospital
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Fujita Takashi
Department Of Biological Sciences Graduate School Of Science The University Of Tokyo
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Fujita Takashi
Department Of Biochemistry The University Of Sydney
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Yasutomi Chigusa
Department Of Pharmacology Faculty Of Pharmaceutical Sciences Setsunan University
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Fujita Takashi
Department Of Anesthesiology Suwa Red Cross Hospital
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