Participation of oxidative stress in the process of osteoclast differentiation

Suda, Naoto; Morita, Ikuo; Kuroda, Takayuki; Murota, Sei‐itsu

doi:10.1016/0304-4165(93)90116-p

Cited by 120 publications

(74 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…ROS are important for stimulating osteoclast differentiation and function [21][22][23][24]. The effect of high glucose on intracellular ROS production in RAW264.7 cultures was analyzed using the peroxide-sensitive DCF-DA probe.…”

Section: High D-glc Inhibits Ros Production In Raw2647 Culturesmentioning

confidence: 99%

“…Binding of RANKL to its cognant receptor on osteoclast precursors leads to activation of NF-κB that is required for osteoclast differentiation [19,20]. Reactive oxygen species (ROS) are also crucial for RANKL-induced osteoclastogenesis [21][22][23][24] and NF-κB is among the redoxsensitive cell signaling pathways [25][26][27]. Recent studies indicate that ROS such as hydrogen peroxide produced in BMM cells stimulate osteoclast differentiation, whereas decreasing the level of ROS reverses RANKL responses [28].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis

Wittrant

Gorin

Woodruff

et al. 2008

Bone

146

View full text Add to dashboard Cite

Diabetes is a chronic disease associated with hyperglycemia and altered bone metabolism that may lead to complications including osteopenia, increased risk of fracture and osteoporosis. Hyperglycemia has been implicated in the pathogenesis of diabetic bone disease; however, the biologic effect of glucose on osteoclastogenesis is unclear. In the present study, we examined the effect of high D(+)glucose (D-Glc) and L(−)glucose (L-Glc; osmotic control) on RANKL-induced osteoclastogenesis using RAW264.7 cells and Bone Marrow Macrophages (BMM) as models. Cells were exposed to sustained high glucose levels to mimic diabetic conditions. Osteoclast formation was analyzed using tartrate resistant acid phosphatase (TRACP) assay, expression of calcitonin receptor (CTR) and cathepsin K mRNAs, and cultures were examined for reactive oxygen species (ROS) using dichlorodihydrofluorescein diacetate (DCF-DA) fluorescence, caspase-3 and Nuclear Factor kappaB (NF-κB) activity. Cellular function was assessed using a migration assay. Results show, for the first time, that high D-Glc inhibits osteoclast formation, ROS production, caspase-3 activity and migration in response to RANKL through a metabolic pathway. Our findings also suggest that high D-Glc may alter RANKL-induced osteoclast formation by inhibiting redox-sensitive NF-κB activity through an anti-oxidative mechanism. This study increases our understanding of the role of glucose in diabetes-associated bone disease. Our data suggest that high glucose levels may alter bone turnover by decreasing osteoclast differentiation and function in diabetes and provide new insight into the biologic effects of glucose on osteoclastogenesis.

show abstract

Section: High D-glc Inhibits Ros Production In Raw2647 Culturesmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis

Wittrant

Gorin

Woodruff

et al. 2008

Bone

146

View full text Add to dashboard Cite

show abstract

“…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

View full text Add to dashboard Cite

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.

show abstract

“…In fact, other antioxidants fail to stimulate differentiation, but some oxidants do (201,268). Indeed, increased free radical generation and accumulation of oxidation reaction products have repeatedly been observed during the differentiation and development of a wide variety of cells and organisms (205,243,(271)(272)(273)(274)(275)(276)(277). Itwas our observations inPhysarum (201,205) and Friend cell leukemia (268) that led us to postulate that an upsurge of oxidant production rather than increased antioxidant defenses were stimulatory to pathways involved in differentiation (36,192,201,205,268).…”

Section: Su Peroxide Dism Utase and Oxidative Stress In Development Amentioning

confidence: 86%

Oxidative stress and superoxide dismutase in development, aging and gene regulation

Allen

1998

AGE

View full text Add to dashboard Cite

Free radicals and other reactive oxygen species are produced in the metabolic pathways of aerobic cells and affect a number of biological processes. Oxidation reactions have been postulated to play a role in aging, a number of degenerative diseases, differentiation and development as well as serving as subcellular messengers in gene regulatory and signal transduction pathways. The discovery of the activity of superoxide dismutase is a seminal work in free radical biology, because it established that free radicals were generated by ceils and because it made removal of a specific free radical substance possible for the first time, which greatly accelerated research in this area. In this review, the role of reactive oxygen in aging, amyotrophic lateral sclerosis (a neurodegenerative disease), development, differentiation, and signal transduction are discussed. Emphasis is also given to the role of superoxide dismutases in these phenomena.

show abstract

Participation of oxidative stress in the process of osteoclast differentiation

Cited by 120 publications

References 22 publications

High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis

High d(+)glucose concentration inhibits RANKL-induced osteoclastogenesis

Salvianolic acid B stimulates osteogenesis in dexamethasone-treated zebrafish larvae

Oxidative stress and superoxide dismutase in development, aging and gene regulation

Contact Info

Product

Resources

About