ArticleScientific reports2016
Disruption of c-Kit Signaling in Kit(W-sh/W-sh) Growing Mice Increases Bone Turnover.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- Introduction of Mature Mast Cells into Bone Marrow Alters Bone Metabolism in Growing Mice.International journal of molecular sciences · 2025Article
- Human Bone-Derived Endothelial Cells Mediate Bone Regeneration via Distinct Expression of KIT Ligand.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Role of Mast-Cell-Derived RANKL in Ovariectomy-Induced Bone Loss in Mice.International journal of molecular sciences · 2023Article
- The role of WNT10B in physiology and disease: A 10-year update.Frontiers in cell and developmental biology · 2023Review
- Anabolic actions of parathyroid hormone in a hypophosphatasia mouse model.Osteoporosis international : a journal established as result of cooperation between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA · 2022Article
- Dendritic cell immunoreceptor drives atopic dermatitis by modulating oxidized CaMKII-involved mast cell activation.JCI insight · 2022Article
- Mast Cells in the Mammalian Testis and Epididymis-Animal Models and Detection Methods.International journal of molecular sciences · 2022Review
- Persistent Human KIT Receptor Signaling Disposes Murine Placenta to Premature Differentiation Resulting in Severely Disrupted Placental Structure and Functionality.International journal of molecular sciences · 2020Article
- Article
- C-KIT Expression Distinguishes Fetal from Postnatal Skeletal Progenitors.Stem cell reports · 2020Article
- The Role of Mast Cells in Bone Metabolism and Bone Disorders.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
c-Kit tyrosine kinase receptor has been identified as a regulator of bone homeostasis. The c-Kit loss-of-function mutations in WBB6F1/J-Kit(W/W-v) mice result in low bone mass. However, these mice are sterile and it is unclear whether the observed skeletal phenotype is secondary to a sex hormone deficiency. In contrast, C57BL/6J-Kit(W-sh)/(W-sh) (W(sh)/W(sh)) mice, which carry an inversion mutation affecting the transcriptional regulatory elements of the c-Kit gene, are fertile. Here, we showed that W(sh)/W(sh) mice exhibited osteopenia with elevated bone resorption and bone formation at 6- and 9-week-old. The c-Kit W(sh) mutation increased osteoclast differentiation, the number of committed osteoprogenitors, alkaline phosphatase activity and mineralization. c-Kit was expressed in both osteoclasts and osteoblasts, and c-Kit expression was decreased in W(sh)/W(sh)osteoclasts, but not osteoblasts, suggesting an indirect effect of c-Kit on bone formation. Furthermore, the osteoclast-derived coupling factor Wnt10b mRNA was increased in W(sh)/W(sh) osteoclasts. Conditioned medium from W(sh)/W(sh) osteoclasts had elevated Wnt10b protein levels and induced increased alkaline phosphatase activity and mineralization in osteoblast cultures. Antagonizing Wnt10b signaling with DKK1 or Wnt10b antibody inhibited these effects. Our data suggest that c-Kit negatively regulates bone turnover, and disrupted c-Kit signaling couples increased bone resorption with bone formation through osteoclast-derived Wnt 10 b.
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Registered trials
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