Ciliary Neurotrophic Factor Inhibits Bone Formation and Plays a Sex-Specific Role in Bone Growth and Remodeling

@article{McGregor2010CiliaryNF,
  title={Ciliary Neurotrophic Factor Inhibits Bone Formation and Plays a Sex-Specific Role in Bone Growth and Remodeling},
  author={Narelle E. McGregor and Ingrid J. Poulton and Emma C. Walker and Sueli Pompolo and Julian M W Quinn and T John Martin and Natalie A. Sims},
  journal={Calcified Tissue International},
  year={2010},
  volume={86},
  pages={261-270}
}
Ciliary neurotrophic factor (CNTF) receptor (CNTFR) expression has been described in osteoblast-like cells, suggesting a role for CNTF in bone metabolism. When bound to CNTF, neuropoietin (NP), or cardiotrophin-like-cytokine (CLC), CNTFR forms a signaling complex with gp130 and the leukemia inhibitory factor receptor, which both play critical roles in bone cell biology. This study aimed to determine the role of CNTFR-signaling cytokines in bone. Immunohistochemistry detected CNTF in osteoblasts… 
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The data reveal that haematopoietic cell-derived CNTF has roles in regulating BM B cell lymphopoiesis and both trabecular and cortical bone, the latter in a sex-dependent manner.
The Primary Function of gp130 Signaling in Osteoblasts Is To Maintain Bone Formation and Strength, Rather Than Promote Osteoclast Formation
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It is concluded that osteocytic gp130 signaling is required for normal trabecular bone mass and proper cortical bone composition and cortical diameter increased to maintain ultimate bone strength, despite a reduction in collagen type 1 production.
GP130 cytokines and bone remodelling in health and disease.
TLDR
The current models of paracrine and endocrine actions of gp130-signalling cytokines inBone remodelling and growth, as well as their impact in pathologic bone remodelling evident in periodontal disease, rheumatoid arthritis, spondylarthropathies and osteoarthritis are discussed.
Contrasting roles of leukemia inhibitory factor in murine bone development and remodeling involve region‐specific changes in vascularization
TLDR
In adult bone undergoing remodeling osteoclast formation was unaffected by LIF deficiency, whereas osteoblast formation and function were both significantly impaired, resulting in osteopenia, whereas an anatomically separate LIF‐dependent pathway regulates osteobasts and adipocyte commitment in bone remodeling.
Leukemia inhibitory factor: A paracrine mediator of bone metabolism
TLDR
The expression patterns of Lif and LIFR in bone, their regulation by physiological and inflammatory agents, as well as cell-specific influences of LIF on osteoblast, osteoclast, chondrocyte, and adipocyte differentiation are described.
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