Oxidative stress in bone remodelling and disease

Wauquier, Fabien; Léotoing, Laurent; Coxam, Véronique; Guicheux, Jérôme; Wittrant, Yohann

doi:10.1016/j.molmed.2009.08.004

Cited by 390 publications

(314 citation statements)

References 78 publications

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“…Oxidative status influences the pathophysiology of mineralised tissues [35] . The role of oxidative injury is one of the mechanisms for the high lipid-induced osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

Sheng

Tang

et al. 2011

Acta Pharmacol Sin

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Aim: To investigate the effects of high cholesterol diet on the development of osteoporosis and the underlying mechanisms in rats. Methods: Female Sprague-Dawley rats were randomly separated into 3 groups: (1) the high cholesterol fed rats were fed a high cholesterol diet containing 77% normal diet food, 3% cholesterol and 20% lard for 3 months; (2) ovariectomised (OVX) rats were bilaterally ovariectomised and fed a standard diet; and (3) the control rats were fed the standard diet. Bone mineral density (BMD) of the rats was measured using dual-energy X-ray absorptiometry. Serum levels of oestradiol (E2), osteocalcin (BGP) and carboxy-terminal collagen crosslinks (CTX) were measured using ELISA. Gene expression profile was determined with microarray. Mouse osteoblast cells (MC3T3-E1) were used for in vitro study. Proliferation, differentiation and oxidative stress of the osteoblasts were investigated using MTT, qRT-PCR and biochemical methods. Results: In high cholesterol fed rats, the femur BMD and serum BGP level were significantly reduced, while the CTX level was significantly increased. DNA microarray analysis showed that 2290 genes were down-regulated and 992 genes were up-regulated in this group of rats. Of these genes, 1626 were also down-regulated and 1466 were up-regulated in OVX rats. In total, 370 genes were up-regulated in both groups, and 976 genes were down-regulated. Some of the down-regulated genes were found to code for proteins involved in the transforming growth factor beta (TGF-β)/bone morphogenic protein (BMP) and Wnt signaling pathways. The up-regulated genes were found to code for IL-6 and Ager with bone-resorption functions. Treatment of MC3T3-E1 cells with cholesterol (12.5-50 μg/mL) inhibited the cell proliferation and differentiation in vitro in a concentration-dependent manner. The treatment also concentration-dependently reduced the expression of BMP2 and Cbfa1, and increased the oxidative injury in MC3T3-E1 cells. Conclusion:The results suggest a close correlation between hypercholesterolaemia and osteoporosis. High cholesterol diet increases the risk of osteoporosis, possible via inhibiting the differentiation and proliferation of osteoblasts.

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“…Oxidative status influences the pathophysiology of mineralised tissues [35] . The role of oxidative injury is one of the mechanisms for the high lipid-induced osteoporosis.…”

Section: Discussionmentioning

confidence: 99%

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

Sheng

Tang

et al. 2011

Acta Pharmacol Sin

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“…Defective coupling of bone formation to resorption plays a key role in the pathogenesis of osteoporosis (Reppe, Datta & Gautvik, 2017; Wauquier, Leotoing, Coxam, Guicheux & Wittrant, 2009). Osteoblasts originate from multipotent mesenchymal progenitors, control bone formation not only by regulating bone matrix synthesis and mineralization but also by orchestrating the process of bone resorption (Yeo et al., 2007).…”

Section: Introductionmentioning

confidence: 99%

Advanced oxidation protein products induce pre‐osteoblast apoptosis through a nicotinamide adenine dinucleotide phosphate oxidase‐dependent, mitogen‐activated protein kinases‐mediated intrinsic apoptosis pathway

et al. 2018

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SummaryOsteoblast apoptosis contributes to age‐related bone loss. Advanced oxidation protein products (AOPPs) are recognized as the markers of oxidative stress and potent inducers of apoptosis. We have demonstrated that AOPP accumulation was correlated with age‐related bone loss. However, the effect of AOPPs on the osteoblast apoptosis still remains unknown. Exposure of osteoblastic MC3T3‐E1 cells to AOPPs caused the excessive generation of reactive oxygen species (ROS) by activating nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. Increased ROS induced phosphorylation of mitogen‐activated protein kinases (MAPKs), which subsequently triggered intrinsic apoptosis pathway by inducing mitochondrial dysfunction, endoplasmic reticulum stress, and Ca2+ overload and eventually leads to apoptosis. Chronic AOPP loading in aged Sprague‐Dawley rats induced osteoblast apoptosis and activated NADPH oxidase signaling cascade, in combination with accelerated bone loss and deteriorated bone microstructure. Our study suggests that AOPPs induce osteoblast apoptosis by the NADPH oxidase‐dependent, MAPK‐mediated intrinsic apoptosis pathway.

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“…Using a female rat model of low and moderate lifetime human exposure to Cd (1 and 5 mg Cd/kg diets, respectively, for up to 24 months), we have revealed that a polyphenol-rich AME may decrease the gastrointestinal absorption and body burden of this xenobiotic (including its accumulation in the liver, kidneys, and bone tissue) [22], as well as significantly prevent disturbances induced by this heavy metal in the bone turnover, and changes in the bone mineral status [23]. Taking into account the pro-oxidative action of Cd and oxidative stress involvement in the mechanisms of this metalʼs toxicity, including osteotoxic action [3,5,[24][25][26][27][28], and the strong antioxidative properties of chokeberry [13,14,[18][19][20], we have hypothesized that the osteoprotective effect reported by us [23] of AME during chronic exposure to Cd may be mediated by the oxidative defense system (the system of defense from oxidative processes and oxidative stress). The aim of the present paper was to investigate this hypothesis.…”

mentioning

confidence: 99%

“…sue oxidative/antioxidative status plays an important role in its physiology and pathology [24][25][26][27]. Oxidative stress has been recognized as one of the mechanisms of osteotoxic Cd action [24,26,27]; however, the exact mechanisms of this metalʼs involvement in the development of bone damage have not been explained until now.…”

mentioning

confidence: 99%

“…Based on the available data [24,26,27], it seems that Cdinduced ROS, which cannot be removed due to their excessive generation, and insufficient antioxidative protection may cause oxidative damage to the macromolecules in the bone tissue and influence the bone turnover. Excessive production and accumulation of ROS has a detrimental impact on bone metabolism via influencing the RANK/RANKL/OPG system [24][25][26]. ROS (particularly H 2 O 2 ) increases the number of osteoclasts and activates their function, leading to a loss of bone mass and a decrease in bone formation via inhibiting osteoblasts generation from osteoprogenitor cells and shortening their survival [25].…”

mentioning

confidence: 99%

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The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

et al. 2016

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!Recently, we demonstrated in a rat model that consumption of a polyphenol-rich extract obtained from the berries of Aronia melanocarpa could protect from cadmium-induced disorders in bone turnover and changes in bone mineral status. The aim of this study was to investigate whether the osteoprotective effect of this extract is mediated by the oxidative defense system. Enzymatic and nonenzymatic antioxidants, total antioxidative and oxidative status, hydrogen peroxide, and markers of oxidative protein, lipid, and DNA damage were determined in bone tissue at the distal femoral epiphysis of female Wistar rats receiving 0.1 % aqueous A. melanocarpa extract (prepared from the lyophilized commercial extract containing 65.74 % of polyphenols) as the only drinking fluid and/or cadmium in the diet (1 and 5 mg/kg) for 3, 10, 17, and 24 months. The total oxidative and antioxidative status of the serum was also evaluated. The administration of A. melanocarpa extract provided significant protection from cadmium-induced oxidative stress in the bone and serum, and from lipid peroxidation and oxidative damage to the protein and DNA in the bone tissue. Numerous correlations were noted between indices of the oxidative/antioxidative bone status and markers of bone metabolism previously assayed in the animals receiving A. melanocarpa extract. The results allow the conclusion that the ability of A. melanocarpa extract to mediate the oxidative defense system and prevent oxidative modifications of protein, lipid, and DNA in the bone tissue plays an important role in its osteoprotective action under exposure to cadmium. The findings provide further evidence supporting our suggestion that chokeberry may be a promising natural agent for protection against the toxic action of cadmium in women chronically exposed to this metal. Abbreviations

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Oxidative stress in bone remodelling and disease

Cited by 390 publications

References 78 publications

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

High cholesterol diet increases osteoporosis risk via inhibiting bone formation in rats

Advanced oxidation protein products induce pre‐osteoblast apoptosis through a nicotinamide adenine dinucleotide phosphate oxidase‐dependent, mitogen‐activated protein kinases‐mediated intrinsic apoptosis pathway

The Mechanism of the Osteoprotective Action of a Polyphenol-Rich Aronia melanocarpa Extract during Chronic Exposure to Cadmium is Mediated by the Oxidative Defense System

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