Fas/CD95 is associated with glucocorticoid-induced osteocyte apoptosis

Kogianni, Giolanta; Mann, V.; Ebetino, Frank H.; Nuttall, Mark; Nijweide, Peter J.; Simpson, Hamish; Noble, Brendon

doi:10.1016/j.lfs.2004.04.048

Cited by 101 publications

(79 citation statements)

References 30 publications

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“…Consistent with these in vivo observations, GCs also promote the apoptosis of osteoblasts and osteocytes in vitro via the activation of caspase-3 (20)(21)(22)(23). In addition, GCs decrease the number of osteoblasts by inhibiting the pool of cells available for differentiation into osteoblasts http://bmbreports.org BMB reports (24).…”

Section: Glucocorticoids and Osteoblastsmentioning

confidence: 53%

New understanding of glucocorticoid action in bone cells

Kim¹

2010

BMB Reports

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Section: Glucocorticoids and Osteoblastsmentioning

confidence: 53%

New understanding of glucocorticoid action in bone cells

Kim¹

2010

BMB Reports

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“…Glucocorticoids have been known to have an effect on bone metabolism [1] and to induce apoptosis in osteoblasts [24,25], osteocytes [26], and numerous lymphoid and myeloid tissues [19,23]. Although the effects of GCs in bone remodeling have been reported, the mechanism of GC-induced apoptosis is poorly understood.…”

Section: Discussionmentioning

confidence: 99%

Glucocorticoid induces apoptosis of osteoblast cells through the activation of glycogen synthase kinase 3β

et al. 2008

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Glucocorticoids (GCs), which play an important role in the normal regulation of bone remodeling, are widely used as anti-inflammatory and chemotherapeutic agents. However, continued exposure to GCs results in osteoporosis, which is partially due to apoptosis of osteoblasts and osteocytes. To understand the mechanism of how GCs induce cell death in osteoblasts, we examined apoptotic effects of dexamethasone (Dex), GC, on MC3T3-E1 osteoblast cells. Results revealed that Dex-induced apoptosis was inhibited by a GC receptor antagonist, mifepristone, and a general caspase inhibitor, Z-VAD-fmk, indicating that Dex induces apoptosis of MC3T3-E1 cells through the pathways involved in GC receptor and caspase. Glycogen synthase kinase 3b (GSK3b) is known to participate in apoptosis signaling in MC3T3-E1 cells. Dex activated both GSK3b and p38-mitogen-activated protein kinase (MAPK). The inhibition of GSK3b by inhibitor (LiCl) or small interference RNA (siRNA) decreased apoptosis. In contrast, the inhibition of p38-MAPK by inhibitor (SB203580) or siRNA did not decrease, but increase apoptosis. These results suggest that Dex-mediated apoptosis of osteoblasts is facilitated by GSK3b, but prevented by p38-MAPK.

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“…Prolonged use of GCs is associated with decreased bone formation, increased resorption and osteonecrosis, through direct and indirect effects on the activity and viability of bone effector cells, osteoblasts and osteoclasts, and osteocytes (3). GCs induce osteoblast and osteocyte apoptosis and promote osteoclastogenesis by increasing levels of RANK-L system (4). Other indirect effects of GCs also play a role in the mechanisms of bone loss such as reduced intestinal calcium absorption and renal calcium wasting and both may lead to a secondary hyperparathyroi dism.…”

Section: Mechanism Of Bone Loss: the Role Of Immunosuppressive Drugs mentioning

confidence: 99%

Bone disease after transplantation: osteoporosis and fractures risk

Kulak

Borba

Kulak

et al. 2014

Arq Bras Endocrinol Metab

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Organ transplantation is the gold standard therapy for several end-stage diseases. Bone loss is a common complication that occurs in transplant recipients. Osteoporosis and fragility fractures are serious complication, mainly in the first year post transplantation. Many factors contribute to the pathogenesis of bone disease following organ transplantation. This review address the mechanisms of bone loss including the contribution of the immunosuppressive agents as well as the specific features to bone loss after kidney, lung, liver, cardiac and bone marrow transplantation. Prevention and management of bone loss in the transplant recipient should be included in their post transplant follow-up in order to prevent fractures. Arq Bras Endocrinol Metab. 2014;58(5):484-92Keywords Transplantation; bone loss; osteoporosis; fractures; immunosuppressive agents RESUMOTransplantes de órgão é terapia padrão-ouro para várias doenças em estágio terminal. Perda óssea é uma complicação comum que ocorre em pacientes transplantados. Osteoporose e fraturas por fragilidade são complicações sérias, principalmente no primeiro ano pós-transplante. Muitos fatores podem contribuir para patogênese da doença óssea nesses pacientes. Esta revisão aborda os mecanismos de perda óssea incluindo o papel dos agentes imunossupressores, bem como os fatores específicos da perda óssea após rim, pulmão, fígado, coração e transplante de medula óssea. A prevenção e o tratamento da perda óssea nos pacientes transplantados devem ser realizados para evitar fraturas. Arq Bras Endocrinol Metab. 2014;58(5):484-92 Descritores

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Fas/CD95 is associated with glucocorticoid-induced osteocyte apoptosis

Cited by 101 publications

References 30 publications

New understanding of glucocorticoid action in bone cells

New understanding of glucocorticoid action in bone cells

Glucocorticoid induces apoptosis of osteoblast cells through the activation of glycogen synthase kinase 3β

Bone disease after transplantation: osteoporosis and fractures risk

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