Intermittent parathyroid hormone administration counteracts the adverse effects of glucocorticoids on osteoblast and osteocyte viability, bone formation, and strength in mice.
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Glucocorticoid receptor signaling in health and diseaseComplex dynamics of transcription regulation.PTH1-34 alleviates radiotherapy-induced local bone loss by improving osteoblast and osteocyte survival.Phosphate interacts with PTHrP to regulate endochondral bone formationDecreased oxidative stress and greater bone anabolism in the aged, when compared to the young, murine skeleton with parathyroid hormone administration.A review of osteocyte function and the emerging importance of sclerostinAn N-ethyl-N-nitrosourea induced corticotropin-releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excessConsequences of daily administered parathyroid hormone on myeloma growth, bone disease, and molecular profiling of whole myelomatous bone.A bisphosphonate that does not affect osteoclasts prevents osteoblast and osteocyte apoptosis and the loss of bone strength induced by glucocorticoids in mice.PTH1 receptor is involved in mediating cellular response to long-chain polyunsaturated fatty acids.PTH1-34 blocks radiation-induced osteoblast apoptosis by enhancing DNA repair through canonical Wnt pathwayAdvances in glucocorticoid-induced osteoporosisEffects of age on parathyroid hormone signaling in human marrow stromal cells.Osteoprotegerin prevents glucocorticoid-induced osteocyte apoptosis in miceGlucocorticoids and tumor necrosis factor α increase oxidative stress and suppress Wnt protein signaling in osteoblastsβ-Ecdysone Augments Peak Bone Mass in Mice of Both Sexes.Prednisolone treatment and restricted physical activity further compromise bone of mdx mice.Glucocorticoid-induced osteoporosis and osteonecrosis.Regulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostinNa+/H+ exchanger regulatory factor 1 (NHERF1) directly regulates osteogenesis.Osteocyte apoptosisEffect of zoledronate on the responses of osteocytes to acute parathyroid hormone.Once-weekly teriparatide improves glucocorticoid-induced osteoporosis in patients with inadequate response to bisphosphonates.Sclerostin-antibody treatment of glucocorticoid-induced osteoporosis maintained bone mass and strength.Vanadate Impedes Adipogenesis in Mesenchymal Stem Cells Derived from Different Depots within Bone.The osteocyte: an endocrine cell ... and more.Proteomic analysis of gingival tissue and alveolar bone during alveolar bone healingReversing bone loss by directing mesenchymal stem cells to bone.Roles of parathyroid hormone (PTH) receptor and reactive oxygen species in hyperlipidemia-induced PTH resistance in preosteoblasts.Parathyroid hormone 1-34 and skeletal anabolic action: The use of parathyroid hormone in bone formation.Glucocorticoid suppression of osteocyte perilacunar remodeling is associated with subchondral bone degeneration in osteonecrosisThe regulation of valvular and vascular sclerosis by osteogenic morphogensOsteocytes: central conductors of bone biology in normal and pathological conditions.Reconciling the effects of inflammatory cytokines on mesenchymal cell osteogenic differentiationMolecular Actions of Glucocorticoids in Cartilage and Bone During Health, Disease, and Steroid Therapy.The Proteasome Inhibitor Bortezomib Maintains Osteocyte Viability in Multiple Myeloma Patients by Reducing Both Apoptosis and Autophagy: A New Function for Proteasome Inhibitors.Black bear parathyroid hormone has greater anabolic effects on trabecular bone in dystrophin-deficient mice than in wild type miceTET3 Mediates Alterations in the Epigenetic Marker 5hmC and Akt pathway in Steroid-Associated Osteonecrosis.The use of intravenous bisphosphonate therapy to treat vertebral fractures due to osteoporosis among boys with Duchenne muscular dystrophy.Control of Bone Anabolism in Response to Mechanical Loading and PTH by Distinct Mechanisms Downstream of the PTH Receptor.
P2860
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P2860
Intermittent parathyroid hormone administration counteracts the adverse effects of glucocorticoids on osteoblast and osteocyte viability, bone formation, and strength in mice.
description
2010 nî lūn-bûn
@nan
2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2010 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2010年の論文
@ja
2010年論文
@yue
2010年論文
@zh-hant
2010年論文
@zh-hk
2010年論文
@zh-mo
2010年論文
@zh-tw
2010年论文
@wuu
name
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@ast
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@en
type
label
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@ast
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@en
prefLabel
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@ast
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@en
P2093
P2860
P356
P1433
P1476
Intermittent parathyroid hormo ...... rmation, and strength in mice.
@en
P2093
Maria Almeida
Paula K Roberson
Robert L Jilka
Robert S Weinstein
Stavros C Manolagas
P2860
P304
P356
10.1210/EN.2009-1488
P407
P577
2010-04-21T00:00:00Z