Glucocorticoids inhibit osteoblast proliferation via transcriptional upregulation of MKP-1: A prime target for the development of novel osteo-anabolic agents

Glucocorticoids inhibit osteoblast proliferation via transcriptional upregulation of MKP-1: A prime target for the development of novel osteo-anabolic agents

Bibliografiska uppgifter
Huvudupphovsmän:	Hulley, P, Horsch, K, De Wet, H, Conradie, M, Langeveldt, C, Hough, F
Materialtyp:	Conference item
Publicerad:	2003

Liknande verk

Rapid inhibitory effects of glucocorticoids on ERK activity and osteoblast proliferation occur via transcriptional upregulation of MKP-1
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Rapid inhibitory effects of glucocorticoids on ERK activity and osteoblast proliferation occur via transcriptional upregulation of MKP-1
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Vanadate protects osteoblasts in vitro and in vivo from glucocorticoid impairment of proliferation
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MKP-1 knockout does not prevent glucocorticoid-induced bone disease in mice.
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Glucocorticoids induce rapid up-regulation of mitogen-activated protein kinase phosphatase-1 and dephosphorylation of extracellular signal-regulated kinase and impair proliferation in human and mouse osteoblast cell lines.
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Vanadate prevents glucocorticoid-induced apoptosis of osteoblasts in vitro and osteocytes in vivo.
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The Role of MKP-1 in the Anti-Proliferative Effects of Glucocorticoids in Primary Rat Pre-Osteoblasts.
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Glucocorticoid-induced osteoporosis in the rat is prevented by the tyrosine phosphatase inhibitor, sodium orthovanadate.
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Mitogen-activated protein kinase phosphatase 1/dual specificity phosphatase 1 mediates glucocorticoid inhibition of osteoblast proliferation.
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The tyrosine phosphatase inhibitor vanadate protects osteoblasts from growth inhibition by glucocorticoids.
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Alternative insulin signalling pathways in osteoblasts
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Alternative insulin signalling pathways in osteoblast cell lines
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Pharmacological estrogen administration causes a FSH-independent osteo-anabolic effect requiring ER alpha in osteoblasts.
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Glucocorticoid transiently upregulates mitochondrial biogenesis in the osteoblast
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The identification of transcriptional targets associated with osteoblast apoptosis signaling in response to growth factor withdrawal
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Corrigendum: Glucocorticoid transiently upregulates mitochondrial biogenesis in the osteoblast
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Regulation of bim in glucocorticoid-mediated osteoblast apoptosis.
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Pathogenesis of glucocorticoid osteoporosis: Role of tyrosine phosphatases
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The BH3-only protein BIM is upregulated in osteoblasts in response to dexamethasone treatment, growth factor deprivation and anoikis
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BIM is a novel regulator of glucocorticoid-induced apoptosis in osteoblasts
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Bim as a potential target in osteoblast survival
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Cynarin attenuates LPS-induced endothelial inflammation via upregulation of the negative regulator MKP-3
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Regulation of the CCL2 gene in pancreatic β-cells by IL-1β and glucocorticoids: role of MKP-1.
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Identification of polymorphisms in the MKP1 gene and their association with bone mineral density in men with asthma
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Scoparone attenuates PD-L1 expression in human breast cancer cells by MKP-3 upregulation
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Anabolic effects and inhibition of interleukin 6 production induced by neridronate on human osteoblasts
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Nonlinearity contributions on critical MKP equation
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MECHANISMS OF OSTEOBLAST INHIBITION BY STEROIDS
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Bim is transcriptionally regulated during induction of apoptosis by growth factor withdrawal in osteoblasts
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Comparison of the Anabolic Effects of Reported Osteogenic Compounds on Human Mesenchymal Progenitor-derived Osteoblasts
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Dose-dependent effect of estrogen suppresses the osteo-adipogenic transdifferentiation of osteoblasts via canonical Wnt signaling pathway.
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Role and regulation of MKP-1 in airway inflammation
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The Unexpected Anabolic Phenotype and Extended Longevity of Skin Fibroblasts after Chronic Glucocorticoid Excess
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Prenatal dexamethasone exposure reduces osteoprogenitor proliferation in mice via histone modifications at the Mkp-1 gene locus
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