Bone Center

Hormonal, paracrine/autocrine as well as mechanical factors regulate Bone remodeling, but multiple neuronal clues appear to be involved as well (PMID: 18410742, PMID: 17440766, PMID: 16132233, PMID: 16054066), in agreement with the homeostatic nature of bone remodeling. We have demonstrated that neurons in the hypothalamus inhibit bone formation by osteoblasts and favor bone resorption by osteoclasts (PMID: 12419242). This function, regulated by the adipocyte-derived hormone leptin, is mediated via the sympathetic nervous system and the beta2-adrenergic receptor expressed by osteoblasts (PMID: 15724149, Figure 1).

Based on these findings, our goal is now to understand the importance of beta2-adrenergic signaling in bone diseases and to determine if one can modify beta2-adrenergic signaling in osteoblasts to improve bone mass. Several mouse genetic models lacking components modulating beta2-adrenergic signaling as well as pharmacological approaches are used in the laboratory to address these questions.

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Hormonal, paracrine/autocrine as well as mechanical factors regulate Bone remodeling, but multiple neuronal clues appear to be involved as well (PMID: 18410742, PMID: 17440766, PMID: 16132233, PMID: 16054066), in agreement with the homeostatic nature of bone remodeling. We have demonstrated that neurons in the hypothalamus inhibit bone formation by osteoblasts and favor bone resorption by osteoclasts (PMID: 12419242). This function, regulated by the adipocyte-derived hormone leptin, is mediated via the sympathetic nervous system and the beta2-adrenergic receptor expressed by osteoblasts (PMID: 15724149, Figure 1). Based on these findings, our goal is now to understand the importance of beta2-adrenergic signaling in bone diseases and to determine if one can modify beta2-adrenergic signaling in osteoblasts to improve bone mass. Several mouse genetic models lacking components modulating beta2-adrenergic signaling as well as pharmacological approaches are used in the laboratory to address these questions. This work is funded by NIH (R21, P.I. F. Elefteriou)

The VUMC Center for Bone Biology is a member of the VUMC Department of Medicine in the Division of Clinical Pharmacology.