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    Sema3A regulates bone-mass accrual through sensory innervations.

    The authors found Sema3A is abundantly expressed in bone, and affected osteoblast differentiation in a cell-autonomous fashion. Sema3a−/− mice had a low bone mass due to decreased bone formation. However, osteoblast-specific Sema3A-deficient mice had normal bone mass, even though the expression of Sema3A in bone was substantially decreased. In contrast, mice lacking Sema3A in neurons had low bone mass, similar to Sema3a−/− mice, indicating that neuron-derived Sema3A is responsible for the observed bone abnormalities independent of the local effect of Sema3A in bone.

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