Cell autonomous requirement of connexin 43 for osteocyte survival: consequences for endocortical resorption and periosteal bone formation. - Wikidata - awgldk - TriplyDB

Cell autonomous requirement of connexin 43 for osteocyte survival: consequences for endocortical resorption and periosteal bone formation.

Cell autonomous requirement of connexin 43 for osteocyte survival: consequences for endocortical resorption and periosteal bone formation.

http://www.wikidata.org/entity/Q35729489

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Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells Gap junctional regulation of signal transduction in bone cells In vitro and in vivo approaches to study osteocyte biology Role of osteocytes in multiple myeloma bone disease Functions of the osteocyte network in the regulation of bone mass Apoptotic osteocytes and the control of targeted bone resorption Connexin 43 hemichannels and intracellular signaling in bone cells Cell Death in Chondrocytes, Osteoblasts, and Osteocytes Physiological mechanisms and therapeutic potential of bone mechanosensing.Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone Silencing the expression of connexin 43 decreases inflammation and joint destruction in experimental arthritis Osteocyte Alterations Induce Osteoclastogenesis in an In Vitro Model of Gaucher Disease Osteocytes mediate the anabolic actions of canonical Wnt/β-catenin signaling in bone.Disruption of the Cx43/miR21 pathway leads to osteocyte apoptosis and increased osteoclastogenesis with aging.Role of TGF-β in a mouse model of high turnover renal osteodystrophy.Parathyroid hormone receptor signaling induces bone resorption in the adult skeleton by directly regulating the RANKL gene in osteocytes.Enhanced periosteal and endocortical responses to axial tibial compression loading in conditional connexin43 deficient mice A new method to investigate how mechanical loading of osteocytes controls osteoblasts Rapidly growing Brtl/+ mouse model of osteogenesis imperfecta improves bone mass and strength with sclerostin antibody treatment Inhibition of GSK-3β rescues the impairments in bone formation and mechanical properties associated with fracture healing in osteoblast selective connexin 43 deficient mice.Connexin 43 channels are essential for normal bone structure and osteocyte viability Evidence for the role of connexin 43-mediated intercellular communication in the process of intracortical bone resorption via osteocytic osteolysis Cx43 and mechanotransduction in bone.Adult Brtl/+ mouse model of osteogenesis imperfecta demonstrates anabolic response to sclerostin antibody treatment with increased bone mass and strength.Activation of HIFa pathway in mature osteoblasts disrupts the integrity of the osteocyte/canalicular network Connexin 43 deficiency desensitizes bone to the effects of mechanical unloading through modulation of both arms of bone remodeling Connexins and pannexins in the skeleton: gap junctions, hemichannels and more Inhibition of osteocyte apoptosis prevents the increase in osteocytic receptor activator of nuclear factor κB ligand (RANKL) but does not stop bone resorption or the loss of bone induced by unloading.Role of connexins and pannexins during ontogeny, regeneration, and pathologies of bone Bisphosphonates improve trabecular bone mass and normalize cortical thickness in ovariectomized, osteoblast connexin43 deficient mice.Defective cancellous bone structure and abnormal response to PTH in cortical bone of mice lacking Cx43 cytoplasmic C-terminus domain.Beyond gap junctions: Connexin43 and bone cell signaling Connexins in the skeleton Osteoblast and osteocyte-specific loss of Connexin43 results in delayed bone formation and healing during murine fracture healing The regulation of runt-related transcription factor 2 by fibroblast growth factor-2 and connexin43 requires the inositol polyphosphate/protein kinase Cδ cascade Absence of Cx43 selectively from osteocytes enhances responsiveness to mechanical force in mice Connexin 43 deficiency attenuates loss of trabecular bone and prevents suppression of cortical bone formation during unloading.Removing or truncating connexin 43 in murine osteocytes alters cortical geometry, nanoscale morphology, and tissue mechanics in the tibia.Deletion of Cx43 from osteocytes results in defective bone material properties but does not decrease extrinsic strength in cortical bone The osteocyte: an endocrine cell ... and more.

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P2860

Cell autonomous requirement of connexin 43 for osteocyte survival: consequences for endocortical resorption and periosteal bone formation.

http://www.wikidata.org/entity/Q35729489

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Journal of Bone and Mineral Research

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Cell autonomous requirement of ...... and periosteal bone formation

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Giovanni Passeri

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Keith W Condon

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Lilian I Plotkin

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Lucas R Brun

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Nathan Farlow

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Nicoletta Bivi

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P2860

Tissue- and site-specific DNA recombination in transgenic mice

Targeted oncogene activation by site-specific recombination in transgenic mice

Connexin 43 (GJA1) mutations cause the pleiotropic phenotype of oculodentodigital dysplasia

Giant osteoclast formation and long-term oral bisphosphonate therapy

Control of bone mass and remodeling by PTH receptor signaling in osteocytes

Mechanical stimulation of bone in vivo reduces osteocyte expression of Sost/sclerostin

Chronic elevation of parathyroid hormone in mice reduces expression of sclerostin by osteocytes: a novel mechanism for hormonal control of osteoblastogenesis

Osteoblast connexin43 modulates skeletal architecture by regulating both arms of bone remodeling

Bone histomorphometry: standardization of nomenclature, symbols, and units. Report of the ASBMR Histomorphometry Nomenclature Committee

Transduction of cell survival signals by connexin-43 hemichannels.

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374-389

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10.1002/JBMR.548

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2

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27

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Matthew R. Allen

Teresita M. Bellido

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2012-02-01T00:00:00Z

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51746237

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22028311

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3271138

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