The Role of Calcium in the Bone Homeostasis and in Skeletal Muscle Regulation (Think of the Role of Hormones and Events During Muscle Contraction)
Other mechanisms by which osteoblast lineage cells control osteoclastogenesis in vivo are being increasingly uncovered, through the use of cell type- and/or stage-specific mutagenesis in mice. For instance, the non-canonical Wnt pathway (Wnt signaling relayed to intracellular responses by mechanisms that are independent of β-catenin actions) between osteoblast-lineage cells and osteoclast precursors appears to regulate bone resorption. Osteoblast-lineage cells express Wnt5a, which activates non-canonical Wnt signaling through receptor tyrosine kinase-like orphan receptor (Ror) proteins such as Ror2, expressed by osteoclast precursors. As a result of this Wnt5a-Ror2 signaling, RANK expression was found to increase and osteoclastogenesis was enhanced.275 Another newly identified mechanism involves osteoblastic expression of semaphorin 3A (Sema3A), a member of the family of secreted and membrane-associated axon guidance molecules that use plexins and neuropilins (Nrp) as their primary receptors; soluble Sema3A produced by osteoblasts was found to exert an osteoprotective effect by inhibiting osteoclast precursor differentiation through the Plexin-A coreceptor Nrp1. In contrast, Sema6D signaling through the receptor Plexin-A on osteoclasts was previously found to promote osteoclast formation and function. Hence, this system’s complexity with multiple interacting ligands and receptors calls for further studies to clarify their precise roles in osteoblast-osteoclast communication.
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