骨芽細胞様細胞MC3T3-E1細胞におけるRANKLおよびOPG遺伝子のα_1およびβアドレナリン受容体を介する発現誘導

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Receptor activator of nuclear factor κB ligand (RANKL) and osteoprotegerin (OPG) produced by bone marrow stromal/osteoblast cells are crucial regulators of osteoclastgenesis and bone resorption. Osteoblastic cells have been demonstrated to express adrenergic receptors. We investigated the expression of α_1- and β-adrenergic receptor subtype genes, and the effect of adrenergic receptor agonists and antagonists on the steady-state mRNA levels of RANKL and OPG in mouse MC3T3-E1 osteoblast-like cells using reverse transcription-polymerase chain reaction (RT-PCR). The mRNA levels of RANKL were rapidly increased by phenylephrine (α_1-agonist) and isoproterenol (β-agonist) as well as epinephrine, and reached a maximal at 2h. They maintained maximal levels until 4h, except that mRNA levels of RANKL induced by isoproterenol had returned to basal levels by 4h. The mRNA levels of OPG were rapidly increased by phenylephrine as well as epinephrine and reached maximal levels at 2h and had returned to basal levels by 4h. In addition, the expression of RANKL and OPG mRNAs induced dose-dependently by phenylephrine, isoproterenol and epinephrine, and phenylephrine and epinephrine, respectively. Prazosin (α_1-antagonist) significantly suppressed the phenylephrine-induced RANKL and OPG mRNA expressions, but yohimbine (α_2-antagonist) and propranolol (β-antagonist) did not. Propranolol significantly inhibited the isoproterenol-induced RANKL mRNA expression, but prazosin and yohimbine did not. MC3T3-E1 cells predominantly expressed α_<1b>-, α_<1d>- and β_2-adrenergic receptor genes. These results suggest that the expression of RANKL and OPG genes in osteoblastic cells is mediated by α_1- and β-, and α_1-adrenergic receptors, respectively.
福岡歯科大学学会の論文
2005-08-25

骨芽細胞様細胞MC3T3-E1細胞におけるRANKLおよびOPG遺伝子のα_1およびβアドレナリン受容体を介する発現誘導

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