Adrenergic stimulation decreases osteoblast oxytocin synthesis

  title={Adrenergic stimulation decreases osteoblast oxytocin synthesis},
  author={Concetta Cuscito and Graziana Colaianni and Roberto Tamma and Giovanni Greco and Stefania Dell'endice and Tony Yuen and Li Sun and Mone Zaidi and Adriana Di Benedetto and Alberta Zambonin Zallone},
  journal={Annals of the New York Academy of Sciences},
Oxytocin (OT) regulates bone mass by inducing the differentiation of osteoblasts to a mature, mineralizing phenotype. We have shown recently that osteoblasts can synthesize OT. In view of known interactions between OT‐ergic and adrenergic neurons in the central nervous system, we questioned whether the negative regulation of osteoblast differentiation by adrenergic nerves was mediated through its suppression of OT synthesis. We first confirmed that α1b and β2 adrenergic receptors were expressed… Expand
Oxytocin effects on osteoblastic differentiation of Bone Marrow Mesenchymal Stem Cells from adult and aging female Wistar rats
A role for OT as an adjuvant to induce osteoblastic differentiation of BMMSCs from aged female rat is suggested. Expand
Effects of fenoterol on the skeletal system depend on the androgen level.
The results indicate the favorable action of fenoterol in conditions of testosterone deficiency, and its destructive influence upon the skeleton in the presence of androgens, and confirm the key role of sympathetic nervous system in the regulation of bone remodeling. Expand
Extracellular Norepinephrine Clearance by the Norepinephrine Transporter Is Required for Skeletal Homeostasis*
It is shown that differentiated osteoblasts, like neurons, express the norepinephrine transporter (NET), exhibit specific NE uptake activity via NET and can catabolize, but not generate, NE, which suggests that drugs antagonizing NET activity, used for the treatment of hyperactivity disorders, may have deleterious effects on bone accrual. Expand
Nocturnal oxytocin secretion is lower in amenorrheic athletes than nonathletes and associated with bone microarchitecture and finite element analysis parameters.
Nocturnal oxytocin secretion is low in AA compared with NA and associated with site-dependent microarchitectural parameters, and may contribute to hypoestrogenemic bone loss in AA. Expand


Regulated production of the pituitary hormone oxytocin from murine and human osteoblasts.
It is surmised that there is a local feed-forward loop in bone marrow through which the OT produced from osteoblasts in response to estrogen acts upon its receptor to exert a potent anabolic action. Expand
Oxytocin is an anabolic bone hormone
Together, the complementary genetic and pharmacologic approaches reveal OT as a novel anabolic regulator of bone mass, with potential implications for osteoporosis therapy. Expand
Leptin Regulates Bone Formation via the Sympathetic Nervous System
A leptin-dependent neuronal regulation of bone formation with potential therapeutic implications for osteoporosis is demonstrated, and the peripheral mediators of leptin antiosteogenic function appear to be neuronal. Expand
Leptin regulation of bone resorption by the sympathetic nervous system and CART
This study establishes that leptin-regulated neural pathways control both aspects of bone remodelling, and demonstrates that integrity of sympathetic signalling is necessary for the increase in bone resorption caused by gonadal failure. Expand
Leptin Inhibits Bone Formation through a Hypothalamic Relay A Central Control of Bone Mass
This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders. Expand
TSH Is a Negative Regulator of Skeletal Remodeling
A role for TSH is defined as a single molecular switch in the independent control of both bone formation and resorption in hyperthyroidism and osteoporosis. Expand
Effects of beta-adrenergic agonists on bone-resorbing activity in human osteoclast-like cells.
It is demonstrated for the first time that beta-adrenergic agonists stimulate bone-resorbing activity in human osteoclast-like multinucleated cells (MNCs). Expand
Functional α1‐ and β2‐adrenergic receptors in human osteoblasts
Examination of the expression of α1‐AR and β2‐AR mRNA and protein and the functional role of adrenergic stimulation in human osteoblasts indicate that both α1B‐ARs andβ2‐ ARs are present and functional in HOBs. Expand
FSH Directly Regulates Bone Mass
It is suggested that high circulating FSH causes hypogonadal bone loss and that Osteoclasts and their precursors possess G(i2alpha)-coupled FSHRs that activate MEK/Erk, NF-kappaB, and Akt to result in enhanced osteoclast formation and function. Expand
Expression of mRNAs for neuropeptide receptors and β-adrenergic receptors in human osteoblasts and human osteogenic sarcoma cells
Observations suggest that neuropeptides and norepinephrine are involved in local regulation of human bone metabolism. Expand