Semaphorin 3A

Xu, Ren

doi:10.4161/cam.27752

Cited by 51 publications

(28 citation statements)

References 59 publications

(73 reference statements)

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“…Bone remodelling consists of two phases, the removal of mineralized bone by osteoclasts, and the formation of new bone by osteoblasts. Therefore, the imbalance of these two cellular functions plays an essential role in skeletal diseases such as osteoporosis (31). Bone-resorbing osteoclasts are formed from a monocyte/macrophage lineage under the strict control of bone-forming osteoblasts (32).…”

Section: Discussionmentioning

confidence: 99%

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Zhang

Ishikawa

Tomoko

et al. 2017

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Section: Discussionmentioning

confidence: 99%

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Zhang

Ishikawa

Tomoko

et al. 2017

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“…Semaphorin 3A (SEMA3A) is the first semaphorin family member identified in vertebrates and ubiquitously expressed in many types of tissue, including brain and bone. While SEMA3A participates in the development of major structures of the nervous system [ 40 ], many studies suggest that SEMA3A also plays a key role in both bone modeling and remodeling [ 40 , 41 , 42 ]. In particular, sensory neuron-derived SEMA3A is necessary for normal bone formation in vivo [ 42 ].…”

Section: Membrane-bound Mediators Of Cell-to-cell Communicationmentioning

confidence: 99%

Osteoblast-Osteoclast Communication and Bone Homeostasis

Kim

Lin

Stavre

et al. 2020

Cells

578

456

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Bone remodeling is tightly regulated by a cross-talk between bone-forming osteoblasts and bone-resorbing osteoclasts. Osteoblasts and osteoclasts communicate with each other to regulate cellular behavior, survival and differentiation through direct cell-to-cell contact or through secretory proteins. A direct interaction between osteoblasts and osteoclasts allows bidirectional transduction of activation signals through EFNB2-EPHB4, FASL-FAS or SEMA3A-NRP1, regulating differentiation and survival of osteoblasts or osteoclasts. Alternatively, osteoblasts produce a range of different secretory molecules, including M-CSF, RANKL/OPG, WNT5A, and WNT16, that promote or suppress osteoclast differentiation and development. Osteoclasts also influence osteoblast formation and differentiation through secretion of soluble factors, including S1P, SEMA4D, CTHRC1 and C3. Here we review the current knowledge regarding membrane bound- and soluble factors governing cross-talk between osteoblasts and osteoclasts.

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“…Sema3A is implicated in the development of osteoporosis through regulation of bone metabolism by removal of mineralized bone and inhibition of the formation of new bone [13]. To further explore the role of Sema3A in bone remodeling, Li et al used Sema3A embedded in matrigel to implant into the metaphysis of proximal tibias in OVX rats [17].…”

Section: Discussionmentioning

confidence: 99%

Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats

Wang

Zhao

et al. 2017

Cell Physiol Biochem

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Purpose: Increasing evidence supported that semaphorin 3A (Sema3A), insulin-like growth factor (IGF)-1 and β-catenin were involved in the development of osteoporosis and diabetes. This study is aimed to evaluate whether Sema3A/IGF-1/β-catenin is directly involved in the alterations of bone microarchitecture and bone strength of diabetic rats. Methods: Diabetic rats were induced by streptozotocin and high fat diet exposure. Bone microarchitecture and strength in the femurs were evaluated by micro-CT scanning, three-point bending examination and the stainings of HE, alizarin red S and safranin O/fast green, respectively. The alterations of lumbar spines microarchitecture were also determined by micro-CT scanning. Western blot and immunohistochemical analyses were used to examine the expression of Sema3A, β-catenin, IGF-1, peroxisome proliferator-activated receptor γ (PPARγ) and cathepsin K in rat tibias. Results: Diabetic rats exhibited decreased trabecular numbers and bone formation, but an increased trabecular separation in the femurs and lumbar spines. Moreover, the increased bone fragility and decreased bone stiffness were evident in the femurs of diabetic rats. Diabetic rats also exhibited a pronounced bone phenotype which manifested by decreased expression of Sema3A, IGF-1 and β-catenin, as well as increased expression of cathepsin K and PPARγ. Conclusions: This study suggests that diabetes could perturb bone loss through the Sema3A/IGF-1/β-catenin pathway. Sema3A deficiency in bone may contribute to upregulation of PPARγ and cathepsin K expression, which further disrupts bone remodeling in diabetic rats.

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Semaphorin 3A

Cited by 51 publications

References 59 publications

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Influence of Mechanical Force on Bone Matrix Proteins in Ovariectomised Mice and Osteoblast-like MC3T3-E1 Cells

Osteoblast-Osteoclast Communication and Bone Homeostasis

Diabetes Perturbs Bone Microarchitecture and Bone Strength through Regulation of Sema3A/IGF-1/β-Catenin in Rats

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