Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Shi, Jun; Wang, Long; Zhang, Hongyang; Qiang, Jun; Li, Xiaojie; Shi, Qiyue; Huang, Qiang; Gao, Bo; Han, Yuehu; Guo, Kai; Liu, Jian; Liu, Yang; Luo, Zhuojing

doi:10.1016/j.bone.2015.06.014

Cited by 80 publications

(68 citation statements)

References 49 publications

(57 reference statements)

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“…In this case, it was suggested that autophagy would act as a protective factor reducing cell stress, increasing the formation and viability of osteoclasts. [71][72][73] Deletions in genes encoding key proteins in the formation of the autophagosome (ATG5, ATG7, ATG4B and LC3) have been shown to cause changes in the brush border formation of osteoclasts, and, consequently, to reduce bone resorption and increase bone volume, thus preventing bone loss in mice after ovariectomy. 65 Some authors suggest that inhibition of autophagy in osteoclasts may serve as a possible therapeutic mechanism against bone diseases in which there is an excessive increase in bone resorption.…”

Section: Role Of Autophagy In Bone Biologymentioning

confidence: 99%

Osteoporosis and autophagy: What is the relationship?

Florencio‐Silva

Sasso

Simões

et al. 2017

Rev. Assoc. Med. Bras.

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Autophagy is a survival pathway wherein non-functional proteins and organelles are degraded in lysosomes for recycling and energy production. Therefore, autophagy is fundamental for the maintenance of cell viability, acting as a quality control process that prevents the accumulation of unnecessary structures and oxidative stress. Increasing evidence has shown that autophagy dysfunction is related to several pathologies including neurodegenerative diseases and cancer. Moreover, recent studies have shown that autophagy plays an important role for the maintenance of bone homeostasis. For instance, in vitro and animal and human studies indicate that autophagy dysfunction in bone cells is associated with the onset of bone diseases such as osteoporosis. This review had the purpose of discussing the issue to confirm whether a relationship between autophagy dysfunction and osteoporosis exits.

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Section: Role Of Autophagy In Bone Biologymentioning

confidence: 99%

Osteoporosis and autophagy: What is the relationship?

Florencio‐Silva

Sasso

Simões

et al. 2017

Rev. Assoc. Med. Bras.

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“…Excessive GCsevoked production of ROS and oxidative stress were observed in a variety of cell types [13,14]. By contrast, recent evidence also suggests a protective role of hormonal therapy against oxidative damage to cells [15].…”

Section: Controlmentioning

confidence: 99%

Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells

Shymanskyy¹,

Lisakovska²,

Mazanova³

et al. 2016

Ukr.Biochem.J.

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“…In skeletal tissue, excessive ROS generation directly promotes apoptosis of osteoblasts and osteocytes [6][7][8] , and ROS-elicited OS also contributes to increased osteoclast differentiation and function [9,10] . Furthermore, studies confirm that GC elicits increased ROS production and subsequent OS in skeletal tissue [11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Salvianolic acid B stimulates osteogenesis in dexamethasone-treated zebrafish larvae

et al. 2016

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Aim: Our previous studies show that salvianolic acid B (Sal B) promotes osteoblast differentiation and matrix mineralization. In this study, we evaluated the protective effects of Sal B on the osteogenesis in dexamethasone (Dex)-treated larval zebrafish, and elucidated the underlying mechanisms. Methods: At 3 d post fertilization, wild-type AB zebrafish larvae or bone transgenic tg (sp7:egfp) zebrafish larvae were exposed to Sal B, Dex, or a mixture of Dex+Sal B for 6 d. Bone mineralization in AB strain larval zebrafish was assessed with alizarin red staining, and osteoblast differentiation in tg (sp7:egfp) larval zebrafish was examined with fluorescence scanning. The expression of osteoblastspecific genes in the larvae was detected using qRT-PCR assay. The levels of oxidative stress markers (ROS and MDA) in the larvae were also measured. Results: Exposure to Dex (5-20 μmol/L) dose-dependently decreased the bone mineralization area and integral optical density (IOD) in wild-type AB zebrafish larvae and the osteoblast fluorescence area and IOD in tg (sp7:egfp) zebrafish larvae. Exposure to Dex (10 μmol/L) significantly reduced the expression of osteoblast-specific genes, including runx2a, osteocalcin (OC), alkaline phosphatase (ALP) and osterix (sp7), and increased the accumulation of ROS and MDA in the larvae. Co-exposure to Sal B (0.2-2 μmol/L) dosedependently increased the bone mineralization area and IOD in AB zebafish larvae and osteoblast fluorescence in tg (sp7:egfp) zebrafish larvae. Co-exposure to Sal B (2 μmol/L) significantly attenuated deleterious alterations in bony tissue and oxidative stress in both Dex-treated AB zebafish larvae and tg (sp7:egfp) zebrafish larvae. Conclusion: Sal B stimulates bone formation and rescues GC-caused inhibition on osteogenesis in larval zebrafish by counteracting oxidative stress and increasing the expression of osteoblast-specific genes. Thus, Sal B may have protective effects on bone loss trigged by GC.

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Glucocorticoids: Dose-related effects on osteoclast formation and function via reactive oxygen species and autophagy

Cited by 80 publications

References 49 publications

Osteoporosis and autophagy: What is the relationship?

Osteoporosis and autophagy: What is the relationship?

Prednisolone and vitamin D(3) modulate oxidative metabolism and cell death pathways in blood and bone marrow mononuclear cells

Salvianolic acid B stimulates osteogenesis in dexamethasone-treated zebrafish larvae

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