Abstract
Bone remodeling occurs at the bone surface throughout adult life and associates bony quantity and quality. This process is a balance between the osteoblastic bone formation and osteoclastic bone resorption, which cross-talks together. Semaphorin 3A is a membrane-associated secreted protein and regarded as a diffusible axonal chemorepellent, which has been identified in the involvement of bone resorption and formation synchronously. However, the role of Semaphorin 3A in bone homeostasis and diseases remains elusive, in particular the association to osteoblasts and osteoclasts. In this review article, we summarize recent progress of Semaphorin 3A in the bone mass, homeostasis, and diseases and discuss the novel application of nerve-based bone regeneration. This will facilitate the understanding of Semaphorin 3A in skeletal biology and shed new light on the modulation and potential treatment in the bone disorders.
Highlights
Semaphorin 3A (Sema3A), known as C-Collapsin-1, H-Sema III, M-SemD, R-Sema III, Sema-Z1a, is a membrane-associated secreted protein (Behar et al, 1996; Ieda et al, 2007; Fukuda et al, 2013)
Sema3A belongs to the semaphorin family and is firstly identified in the involvement of patterning neuronal connections
Semaphorin protein was firstly found in brain that induces the collapse and stalling of neuronal growth cones, which was named collapsin (Luo et al, 1993)
Summary
Semaphorin 3A (Sema3A), known as C-Collapsin-1, H-Sema III, M-SemD, R-Sema III, Sema-Z1a, is a membrane-associated secreted protein (Behar et al, 1996; Ieda et al, 2007; Fukuda et al, 2013). Osteoclastic-like multinucleated cells from bone marrow have been demonstrated to express the ligands and receptors of Sema3A already (Koshihara et al, 1999; Togari et al, 2000). Hayashi et al (2012) observed a severe osteopenic phenotype in Sema3a knock-out mice (Sema3a−/− mice), which was caused by a decrease in the osteoblastic bone formation and an increase in osteoclastic bone resorption.
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