Increased GABA Transport Activity in Rat Calvarial Osteoblasts Cultured under Hyperglycemic Conditions(Pharmacology)
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概要
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Several independent lines of evidence indicate the direct impairment by extracellular glucose at high concentrations of different osteoblastic functions with a marked decrease in bone mass toward osteoporosis, while the underlying mechanisms are not well clarified to date. We have previously demonstrated the functional expression of the neural amino acid γ-aminobutyric acid (GABA) signaling system including betaine/GABA transporter-1 (BGT-1) with a temperature-, sodium- and chloride-dependent activity of [^3H]GABA accumulation in cultured rat calvarial osteoblasts. In this study, therefore, we attempted to demonstrate the possible involvement of BGT-1 isoform in bone dysfunctions due to impaired mineralization in rat calvarial osteoblasts cultured under hyperglycemic conditions. No significant change was seen in [^3H]GABA accumulation in osteoblasts cultured for 7d in vitro (DIV) under hyperglycemic conditions (glucose=25.5-50.5mM) compared to those cultured in normoglycemic (glucose=5.5mM) and hyperosmotic (mannitol=25.5-50.5mM) conditions. In osteoblasts cultured for 14 DIV under hyperglycemic conditions, however, [^3H]GABA accumulation was significantly increased compared to those cultured under normoglycemic and hyperosmotic conditions. Kinetic analysis revealed that hyperglycemic cultivation resulted in a significant increase in V_<max> values from 2.85nmol/min/mg protein for normoglycemic conditions to 4.17nmol/min/mg protein for hyperglycemic conditions without affecting K_m values. However, experimental hyperglycemia did not significantly affect the expression of mRNA for BGT-1 isoform by osteoblasts. These results suggest that GABA transport system may at least in part play a role in pathological malfunctions and abnormalities through a mechanism not directly related to gene expression in osteoblasts under hyperglycemia.
- 公益社団法人日本薬学会の論文
- 2006-02-01
著者
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HINOI Eiichi
Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Gradu
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YONEDA Yukio
Laboratory of Molecular Pharmacology, Division of Pharmaceutical Sciences, Kanazawa University Gradu
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Yoneda Yukio
Lab. Of Molecular Pharmacology Div. Of Pharmaceutical Sciences Kanazawa Univ. Graduate School Of Nat
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Yoneda Yukio
Laboratory Of Molecular Pharmacology Division Of Pharmaceutical Sciences Kanazawa University Graduat
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Hinoi Eiichi
Lab. Of Molecular Pharmacology Div. Of Pharmaceutical Sciences Kanazawa Univ. Graduate School Of Nat
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Hinoi Eiichi
Laboratory Of Molecular Pharmacology Division Of Pharmaceutical Sciences Kanazawa University Graduat
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Hinoi Eiichi
Laboratory Of Molecular Pharmacology Kanazawa University Graduate School Of Natural Science And Tech
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FUJIMORI Sayumi
Laboratory of Molecular Pharmacology, Kanazawa University Graduate School of Natural Science and Tec
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OSAWA Masato
Laboratory of Molecular Pharmacology, Kanazawa University Graduate School of Natural Science and Tec
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IEMATA Mika
Laboratory of Molecular Pharmacology, Kanazawa University Graduate School of Natural Science and Tec
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Yoneda Yukio
Laboratory Of Molecular Pharmacology Kanazawa University Graduate School Of Natural Science And Tech
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Iemata Mika
Laboratory Of Molecular Pharmacology Kanazawa University Graduate School Of Natural Science And Tech
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Osawa Masato
Laboratory Of Molecular Pharmacology Kanazawa University Graduate School Of Natural Science And Tech
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Fujimori Sayumi
Laboratory Of Molecular Pharmacology Kanazawa University Graduate School Of Natural Science And Tech
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