Intermittent parathyroid hormone administration converts quiescent lining cells to active osteoblasts. - Wikidata - awgldk - TriplyDB

Intermittent parathyroid hormone administration converts quiescent lining cells to active osteoblasts.

Intermittent parathyroid hormone administration converts quiescent lining cells to active osteoblasts.

http://www.wikidata.org/entity/Q36486277

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Effects of PTH on osteocyte function Parathyroid Hormone Induces Bone Cell Motility and Loss of Mature Osteocyte Phenotype through L-Calcium Channel Dependent and Independent Mechanisms Hyperbaric Oxygen Promotes Proximal Bone Regeneration and Organized Collagen Composition during Digit Regeneration Osteocyte-specific deletion of Fgfr1 suppresses FGF23 Parathyroid hormone: anabolic and catabolic actions on the skeleton Quiescent Bone Lining Cells Are a Major Source of Osteoblasts During Adulthood.Prostaglandin E2 acts via bone marrow macrophages to block PTH-stimulated osteoblast differentiation in vitro.Treatment with N- and C-terminal peptides of parathyroid hormone-related protein partly compensate the skeletal abnormalities in IGF-I deficient mice.Cyclooxygenase-2 suppresses the anabolic response to PTH infusion in mice.Teriparatide (PTH 1-34) treatment increases peripheral hematopoietic stem cells in postmenopausal women.Lipoprotein receptor-related protein 6 is required for parathyroid hormone-induced Sost suppression.Loss of Gsα in the Postnatal Skeleton Leads to Low Bone Mass and a Blunted Response to Anabolic Parathyroid Hormone Therapy Intermittent PTH administration and mechanical loading are anabolic for periprosthetic cancellous bone.PTH Promotes Bone Anabolism by Stimulating Aerobic Glycolysis via IGF Signaling.Parathyroid hormone (PTH)/PTH-related peptide type 1 receptor (PPR) signaling in osteocytes regulates anabolic and catabolic skeletal responses to PTH.Short-term intermittent administration of parathyroid hormone facilitates osteogenesis by different mechanisms in cancellous and cortical bone Navigating the bone marrow niche: translational insights and cancer-driven dysfunction.Resorption controls bone anabolism driven by parathyroid hormone (PTH) receptor signaling in osteocytes Roles of parathyroid hormone (PTH) receptor and reactive oxygen species in hyperlipidemia-induced PTH resistance in preosteoblasts.Bone marrow mesenchymal stem cells and TGF-β signaling in bone remodeling.Parathyroid hormone 1-34 and skeletal anabolic action: The use of parathyroid hormone in bone formation.Bone biology and anabolic therapies for bone: current status and future prospects.Estrogen receptors alpha and beta in bone.Treating osteoporosis by targeting parathyroid hormone to bone.The reversal phase of the bone-remodeling cycle: cellular prerequisites for coupling resorption and formation.Co-administration of antiresorptive and anabolic agents: a missed opportunity.Osteogenic programs during zebrafish fin regeneration.Estrogen Regulates Bone Turnover by Targeting RANKL Expression in Bone Lining Cells.Parathyroid Hormone-Related Protein, Its Regulation of Cartilage and Bone Development, and Role in Treating Bone Diseases.Sclerostin Antibody Administration Converts Bone Lining Cells Into Active Osteoblasts.Heterotrimeric G proteins in the control of parathyroid hormone actions.N-cadherin restrains PTH repressive effects on sclerostin/SOST by regulating LRP6-PTH1R interaction.Osteogenic Factor Runx2 Marks a Subset of Leptin Receptor-Positive Cells that Sit Atop the Bone Marrow Stromal Cell Hierarchy.Tissue-level mechanisms responsible for the increase in bone formation and bone volume by sclerostin antibody.Combination therapy with PTH and DBM cannot heal a critical sized murine femoral defect.New Insights Into the Local and Systemic Functions of Sclerostin: Regulation of Quiescent Bone Lining Cells and Beige Adipogenesis in Peripheral Fat Depots.Parathyroid hormone regulates fates of murine osteoblast precursors in vivo.Skeletal Stem Cells: Origins, Functions and Uncertainties.Transforming growth factor-β in stem cells and tissue homeostasis.Energy Metabolism of the Osteoblast: Implications for Osteoporosis.

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Intermittent parathyroid hormone administration converts quiescent lining cells to active osteoblasts.

http://www.wikidata.org/entity/Q36486277

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2012 nî lūn-bûn

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Intermittent parathyroid hormo ...... g cells to active osteoblasts.

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Intermittent parathyroid hormo ...... g cells to active osteoblasts.

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Intermittent parathyroid hormo ...... g cells to active osteoblasts.

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Intermittent parathyroid hormo ...... g cells to active osteoblasts.

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Intermittent parathyroid hormo ...... g cells to active osteoblasts.

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Journal of Bone and Mineral Research

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Intermittent parathyroid hormo ...... g cells to active osteoblasts.

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P2093

Chan Soo Shin

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Henry M Kronenberg

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Jae-Yeon Yang

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Jung-Eun Kim

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Kevin J Barry

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Martin Selig

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Paola Divieti Pajevic

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Sang Wan Kim

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Wook-Young Baek

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P2860

Generalized lacZ expression with the ROSA26 Cre reporter strain

Mesenchymal and haematopoietic stem cells form a unique bone marrow niche

Osteoblast precursors, but not mature osteoblasts, move into developing and fractured bones along with invading blood vessels.

Molecular and cellular mechanisms of the anabolic effect of intermittent PTH

The parathyroid hormone/parathyroid hormone-related peptide receptor coordinates endochondral bone development by directly controlling chondrocyte differentiation.

Quantifying osteoblast and osteocyte apoptosis: challenges and rewards.

Intermittent PTH stimulates periosteal bone formation by actions on post-mitotic preosteoblasts

Targeted ablation of the PTH/PTHrP receptor in osteocytes impairs bone structure and homeostatic calcemic responses

Bone lining cells: structure and function.

The bone lining cell: a distinct phenotype?

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10.1002/JBMR.1665

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10

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27

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2012-10-01T00:00:00Z

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225059126

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22623172

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