Inpp4b as a regulator of bone mass

Osteoclasts are the major cell type involved in bone resorption. Unbalanced increase of osteoclasts activity decreases bone mass and favors osteoporosis. The authors of this study [1] identified a regulator of osteoclastogenesis, inositol polyphosphate 4-phosphatase type 2 α (Inpp4bα), a member of the PI3 kinase signaling pathway.

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Sympathetic control of bone mass is regulated by osteopontin

Activation of the sympathetic nervous system is known to reduce bone mass through mechanisms that remain unclear. Using cell-based studies and murine genetics, the authors [1] showed that osteopontin (OPN) is required for the sympathetic activity on bone metabolism.

Osteopontin is a cytokine and one of the major members of noncollagenous extracellular matrix proteins of bone.
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Sirt1 is a regulator of bone mass and a repressor of Sost encoding Sclerostin

Sirtuin 1 (Sirt1) is a member of the sirtuin family. The sirtuins are a family of evolutionarily highly conserved protein deacetylases that were found to regulate the lifespan in lower species and key cellular and metabolic functions in mammals. Sirt1 is a deacetylase that plays an important role in metabolism and in age-associated diseases.

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Osteoprotegerin prevents glucocorticoid-induced osteocytes apoptosis in mice

Glucocorticoid excess has negative effects on bone strength, as previously reported in numerous studies. This excess leads to a decreased production of osteoblasts and osteoclasts, associated with a prolongation of osteoclast lifespan. Moreover, glucocorticoid excess leads to massive osteoblast and osteocyte apoptosis associated with an alteration of the lacunar-canalicular network. These combined effects induce an important loss of bone mass and strength. RANKL is well known to promote osteoclast differentiation leading to bone loss. In this study, the authors [1] tested the effect of osteoprotegerin (OPG-Fc), a RANKL decoy receptor, on the decrease of bone strength induced by glucocorticoid excess..

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Macrophage-CSF is a potent stimulator of osteoclast resorbing activity

Macrophage-CSF (M-CSF) is reported to enhance mature osteoclast survival and motility, but its role in the regulation of bone resorption is unclear. The authors of this study [1] analyzed short-term culture of mature osteoclasts in the presence or in absence of the osteoclast differentiation factor RANK ligand (RANKL) with or without M-CSF treatment.

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