Expression of mRNAs for neuropeptide receptors and β-adrenergic receptors in human osteoblasts and human osteogenic sarcoma cells

Togari, Akifumi; Arai, M.; Mizutani, Shigeki; Koshihara, Yasuko; Nagatsu, Toshiharu

doi:10.1016/s0304-3940(97)00649-6

Cited by 190 publications

(121 citation statements)

References 26 publications

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“…Consistent with these observations, several investigators have reported the expression of b2-adrenergic receptors, and less consistently b1-adrenergic receptors, in human periosteal osteoblasts, osteosarcoma-derived osteoblast-like cells, rat and mouse osteoblastic cells, (5,(9)(10)(11) and also in human osteoclast-like cells. (12,13) Adrenergic agonists stimulated bone resorption in neonatal mouse calvariae, (10) increased osteoclastogenesis in vitro, and promoted the osteoblastic production of interleukin 6 (IL-6) and receptor activator of NF-kB ligand (RANKL)-two osteoclast-activating cytokines. (14,15) In turn, b2-adrenergic receptor deficient (Adrb2 À/À ) mice were characterized by increased cancellous bone volume and bone formation rate (BFR) compared to their wild-type (WT) as they age (ie, by 6 months of age) and also following estrogen-deficiency, at least when ovariectomy was performed during growth (ie, by 1 month of age).…”

supporting

confidence: 59%

Deletion of β-adrenergic receptor 1, 2, or both leads to different bone phenotypes and response to mechanical stimulation

Pierroz¹,

Bonnet²,

Bianchi³

et al. 2012

Journal of Bone and Mineral Research

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As they age, mice deficient for the b2-adrenergic receptor (Adrb2 À/À ) maintain greater trabecular bone microarchitecture, as a result of lower bone resorption and increased bone formation. The role of b1-adrenergic receptor signaling and its interaction with b2-adrenergic receptor on bone mass regulation, however, remains poorly understood. We first investigated the skeletal response to mechanical stimulation in mice deficient for b1-adrenergic receptors and/or b2-adrenergic receptors. Upon axial compression loading of the tibia, bone density, cancellous and cortical microarchitecture, as well as histomorphometric bone forming indices, were increased in both Adrb2 À/À and wild-type (WT) mice, but not in Adrb1 À/À nor in Adrb1b2 À/À mice. Moreover, in the unstimulated femur and vertebra, bone mass and microarchitecture were increased in Adrb2 À/À mice, whereas in Adrb1 À/À and Adrb1b2 À/À double knockout mice, femur bone mineral density (BMD), cancellous bone volume/total volume (BV/TV), cortical size, and cortical thickness were lower compared to WT. Bone histomorphometry and biochemical markers showed markedly decreased bone formation in Adrb1b2 À/À mice during growth, which paralleled a significant decline in circulating insulin-like growth factor 1 (IGF-1) and IGF-binding protein 3 (IGF-BP3). Finally, administration of the b-adrenergic agonist isoproterenol increased bone resorption and receptor activator of NF-kB ligand (RANKL) and decreased bone mass and microarchitecture in WT but not in Adrb1b2 À/À mice. Altogether, these results demonstrate that b1-and b2-adrenergic signaling exert opposite effects on bone, with b1 exerting a predominant anabolic stimulus in response to mechanical stimulation and during growth, whereas b2-adrenergic receptor signaling mainly regulates bone resorption during aging. ß

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supporting

confidence: 59%

Deletion of β-adrenergic receptor 1, 2, or both leads to different bone phenotypes and response to mechanical stimulation

Pierroz¹,

Bonnet²,

Bianchi³

et al. 2012

Journal of Bone and Mineral Research

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“…PACAP has been detected in cartilage canals from newborn pigs (Strange-Vognsen et al, 1997), and functional receptors are expressed in human and mouse osteoblasts as well as in rat and mouse osteoclasts (Togari et al, 1997;Lundberg et al, 2000;Ransjö et al, 2000). Consistent with these observations, PACAP increases cAMP formation in mouse calvarial bones (Lerner et al, 1994) and synergizes with the proinflammatory bone-resorbing cytokine IL-1␤ in osteoblasts to promote the production of IL-6, another well known stimulator of bone resorption (Persson and Lerner, 2005).…”

Section: Effects Of Pituitary Adenylate Cyclase-activating Polypepmentioning

confidence: 55%

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

et al. 2009

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“…Previous studies, including ours, showed that the mRNAs of the ␣1-AR and ␤-AR subtypes were expressed in mouse and human osteoblasts (30,31). ␤-AR signaling in osteoblasts has been shown to stimulate bone resorption by up-regulating receptor activator of nuclear factor B ligands (Rankl).…”

Section: Discussionmentioning

confidence: 80%

α1-Adrenergic Receptor Signaling in Osteoblasts Regulates Clock Genes and Bone Morphogenetic Protein 4 Expression through Up-regulation of the Transcriptional Factor Nuclear Factor IL-3 (Nfil3)/E4 Promoter-binding Protein 4 (E4BP4)

Hanabusa

Tanaka

Togari

2014

Journal of Biological Chemistry

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Background:The physiological role of ␣1-adrenergic receptor (AR) signaling in bone is largely unknown. Results: ␣1-AR signaling negatively regulates Bmp4 expression by up-regulating the transcriptional factor Nfil3/E4BP4 in osteoblasts. Conclusion: ␣1-AR signaling regulates clock genes and Bmp4 expression in osteoblasts. Significance: The regulation of clock genes by ␣1-AR signaling in osteoblasts may contribute to the physiological significance of the circadian clockwork in bone metabolism.

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Expression of mRNAs for neuropeptide receptors and β-adrenergic receptors in human osteoblasts and human osteogenic sarcoma cells

Cited by 190 publications

References 26 publications

Deletion of β-adrenergic receptor 1, 2, or both leads to different bone phenotypes and response to mechanical stimulation

Deletion of β-adrenergic receptor 1, 2, or both leads to different bone phenotypes and response to mechanical stimulation

Pituitary Adenylate Cyclase-Activating Polypeptide and Its Receptors: 20 Years after the Discovery

α1-Adrenergic Receptor Signaling in Osteoblasts Regulates Clock Genes and Bone Morphogenetic Protein 4 Expression through Up-regulation of the Transcriptional Factor Nuclear Factor IL-3 (Nfil3)/E4 Promoter-binding Protein 4 (E4BP4)

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