RANKL signaling in bone marrow mesenchymal stem cells negatively regulates osteoblastic bone formation

Chen, Xiao; Zhi, Xiao; Wang, Jun; Su, Jiacan

doi:10.1038/s41413-018-0035-6

Cited by 116 publications

(112 citation statements)

References 27 publications

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“…Bone homeostasis was maintained by bone‐resorbing osteoclasts and bone‐forming osteoblasts . RANKL has been revealed to be associated with osteoporosis in postmenopausal women . An experiment had stated that RANKL can stimulate osteoclast formation .…”

Section: Discussionmentioning

confidence: 99%

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Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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Here, we aim at exploring the effect of CST5 on bone resorption and activation of osteoclasts in osteoporosis (OP) rats through the NF‐κB pathway. Microarray analysis was used to screen the OP‐related differentially expressed genes. Osteoporosis was induced in rats by intragastric retinoic acid administration. The serum levels of tartrate‐resistant acid phosphatase (TRAP), bone alkaline phosphatase (BALP) and osteocalcin (OC) and the expression of CD61 on the surface of osteoclasts were examined. The number of osteoclasts and the number and area of resorption pits were detected. Besides, the pathological changes and bone mineral density in bone tissues of rats were assessed. Also, the relationship between CST5 and the NF‐κB pathway was identified through determining the expression of CST5, RANKL, RANK, OPG, p65 and IKB. Poorly expressed CST5 was indicated to affect the OP. CST5 elevation and inhibition of the NF‐κB pathway decreased serum levels of TRAP, BALP and OC and expression of CD61 in vivo and in vitro. In OP rats, CST5 overexpression increased trabecular bones and bone mineral density of bone tissues, but decreased trabecular separation, fat within the bone marrow cavities and the number of osteoclasts through inhibiting the NF‐κB pathway. In vivo experiments showed that CST5 elevation inhibited growth in number and area of osteoclastic resorption pits and restrained osteoclastic bone absorption by inhibiting the NF‐κB pathway. In summary, overexpression of CST5 suppresses the activation and bone resorption of osteoclasts by inhibiting the activation of the NF‐κB pathway.

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Section: Discussionmentioning

confidence: 99%

“…31 RANKL has been revealed to be associated with osteoporosis in postmenopausal women. 32,33 An experiment had stated that RANKL can stimulate osteoclast formation. 34 Another study has illustrated that osteoclastogenesis, bone resorption and osteoclast activities are inhibited through suppression of RANKL pathway.…”

Section: Discussionmentioning

confidence: 99%

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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“…RANKL, a transmembrane protein from the tumor necrosis factor (TNF) superfamily, is able to bind RANK on the surface of osteoclast precursors to trigger osteoclastogenesis . Chen et al discovered that RANKL signaling inhibits osteogenesis by promoting β‐catenin degradation and inhibiting its synthesis, which further suppresses osteogenic differentiation of BMSC. Xiong et al found that soluble RANKL contributes to osteoclast formation in adult mice.…”

Section: Mechanisms Underlying Melatonin's Action On Osteoporosismentioning

confidence: 99%

Melatonin: Another avenue for treating osteoporosis?

Tian

Jiang

et al. 2019

Journal of Pineal Research

111

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Melatonin is a signal molecule that modulates the biological circadian rhythms of vertebrates. Melatonin deficiency is thought to be associated with several disorders, including insomnia, cancer, and cardiovascular and neurodegenerative diseases. Accumulating evidence has also indicated that melatonin may be involved in the homeostasis of bone metabolism. Age‐related reductions in melatonin are considered to be critical factors in bone loss and osteoporosis with aging. Thus, serum melatonin levels might serve as a biomarker for the early detection and prevention of osteoporosis. Compared to conventional antiosteoporosis medicines, which primarily inhibit bone loss, melatonin both suppresses bone loss and promotes new bone formation. Mechanistically, by activating melatonin receptor 2 (MT2), melatonin upregulates the gene expression of alkaline phosphatase (ALP), bone morphogenetic protein 2 (BMP2), BMP6, osteocalcin, and osteoprotegerin to promote osteogenesis while inhibiting the receptor activator of NF‐kB ligand (RANKL) pathway to suppress osteolysis. In view of the distinct actions of melatonin on bone metabolism, we hypothesize that melatonin may be a novel remedy for the prevention and clinical treatment of osteoporosis.

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“…Certain bone anabolic agents, such as PTH, recombinant human growth factors, and platelet-rich concentrates, as well as the major antiresorption medications, namely, bisphosphonates (BPs), have already been showed to be effective in regenerating periodontal bone [1,7]. Moreover, since bone formation and resorption are coupled and coordinated with each other, concurrent application of anabolic and antiresorption agents are introduced in regenerative periodontology very recently [8][9][10]. However, there is a lack of evidence-based studies to answer whether this synergistic way was superior to single application until now.…”

Section: Introductionmentioning

confidence: 99%

Synergistic Application of Platelet-Rich Fibrin and 1% Alendronate in Periodontal Bone Regeneration: A Meta-Analysis

Jiang

Pan

et al. 2019

BioMed Research International

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Periodontal bone regeneration relies on coupled and cooperative bone formation and resorption. Accordingly a novel strategy on concurrent use of platelet-rich fibrin (PRF) (anabolic agent) and 1% alendronate (ALN) (anticatabolic agent) was proposed recently in regenerative periodontal treatment. It was supposed to enhance bone formation and reduce bone resorption simultaneously. However, there is a lack of evidence-based studies to answer whether this concurrent application was superior to single application until now. Besides, concerns on ALN lead to some reservation on this synergistic way. ALN may impair new bone formation and necrotize jaws. Thus, in order to compare the clinical efficacy between PRF plus 1%ALN and PRF alone on periodontal bone regeneration, we performed present systematic review and meta-analysis. Because it is the prerequisite for measuring the combined efficacy of PRF plus 1%ALN, firstly we evaluated the effectiveness of 1%ALN. Our data indicated that adjunctive 1%ALN was effective in promoting periodontal bone repair. Further, PRF plus 1%ALN showed a greater capacity for periodontal regeneration than PRF alone with statistical significance. The findings of this study revealed the promising prospects on synergistic application of bone anabolic agents (PRF) and antiresorption medications (1%ALN) in regenerative periodontal treatment.

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RANKL signaling in bone marrow mesenchymal stem cells negatively regulates osteoblastic bone formation

Cited by 116 publications

References 27 publications

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Up‐regulated CST5 inhibits bone resorption and activation of osteoclasts in rat models of osteoporosis via suppression of the NF‐κB pathway

Melatonin: Another avenue for treating osteoporosis?

Synergistic Application of Platelet-Rich Fibrin and 1% Alendronate in Periodontal Bone Regeneration: A Meta-Analysis

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