The induction of RANKL molecule clustering could stimulate early osteoblast differentiation

Sone, Eri; Noshiro, Daisuke; Ikebuchi, Yuki; Nakagawa, Mami; Khan, Masud; Tamura, Yukihiko; Ikeda, Masaomi; Oki, Meiko; Murali, Ramachandran; Fujimori, Toshihiko; Yoda, Tetsuya; Honma, Masashi; Suzuki, Hiroshi; Ando, Toshio; Aoki, Kazuhiro

doi:10.1016/j.bbrc.2018.12.093

Cited by 18 publications

(12 citation statements)

References 25 publications

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“…Hu et al found that osteoblast-derived VEGF promoted osteoblast differentiation at bone-repair sites [34]. RANKL was considered as the osteoclast development when binding to RANK [35], while RANKL also promoted osteoblast differentiation and osteoblastogenesis [36]. COL1A1 was the mark of osteoclasts, and the expression of COL1A1 was increased during osteoblast differentiation [37].…”

Section: Discussionmentioning

confidence: 99%

Resveratrol promotes osteoblastic differentiation in a rat model of postmenopausal osteoporosis by regulating autophagy

et al. 2020

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Objective: Resveratrol is a natural polyphenolic compound that ameliorates postmenopausal osteoporosis by activating the estrogen receptor. Research has shown that resveratrol exhibits some type of estrogen receptor agonist activity, reducing the risk of breast cancer. However, its mechanism of action remains largely unknown. This study aims to investigate the effect of resveratrol on osteoblastic and osteoclastic differentiation and its potential role in the regulation of autophagy. Methods: Sprague Dawley (SD) rats underwent ovariectomies (OVX) and were administered resveratrol (at 10, 20 or 40 mg/kg/d) for 8 weeks. The calcium content and the bone mineral density (BMD) were measured in the lumbar vertebrae (L3) and the right distal femur-tibia bone region. The osteoblasts and osteoclasts were isolated from rat lumbar vertebrae by enzyme digestion and bone marrow induction, respectively. The cells were then cultured with resveratrol in combination with bafilomycin or leupeptin to inhibit or activate autophagy, respectively. Western blotting was used to assess the differentiation markers and autophagy-related genes in the osteoblasts and osteoclasts. Results: Compared to the sham group, the bone calcium content and BMD were significantly decreased in the OVX group (p < 0.05), while resveratrol attenuated these in a dose-dependent manner. In the osteoblasts, vascular endothelial growth factor (VEGF), and alpha-1 type I collagen (COL1A1) were markedly decreased, and in osteoclasts, the receptor activator of nuclear factor-κB ligand (RANKL) was increased in the OVX group, while resveratrol reversed this pattern in a dose-dependent manner. The inhibition of autophagy in osteoblasts and its activation in osteoclasts was observed in the OVX group. However, with resveratrol, this was reversed in a dosedependent manner. Conclusion: Overall, resveratrol promotes osteoblastic differentiation and suppresses osteoclastic differentiation in a rat model with postmenopausal osteoporosis by regulating autophagy.

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Section: Discussionmentioning

confidence: 99%

Resveratrol promotes osteoblastic differentiation in a rat model of postmenopausal osteoporosis by regulating autophagy

et al. 2020

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“…In parallel, recent papers pointed to an unexpected osteogenic function of RANKL through (at least) two different, not mutually exclusive mechanisms: an autocrine-paracrine loop activated by RANKL binding to its receptor(s) on MSCs (27); and a reverse signaling elicited by osteoclast-derived RANK-expressing extracellular vesicles, which might induce membrane-RANKL clustering on osteoblasts (59, 60). This might represent an additional means for osteoblast-osteoclast crosstalk.…”

Section: Rankl-rank Axis In the Bonementioning

confidence: 99%

The RANKL-RANK Axis: A Bone to Thymus Round Trip

2019

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The identification of Receptor activator of nuclear factor kappa B ligand (RANKL) and its cognate receptor Receptor activator of nuclear factor kappa B (RANK) during a search for novel tumor necrosis factor receptor (TNFR) superfamily members has dramatically changed the scenario of bone biology by providing the functional and biochemical proof that RANKL signaling via RANK is the master factor for osteoclastogenesis. In parallel, two independent studies reported the identification of mouse RANKL on activated T cells and of a ligand for osteoprotegerin on a murine bone marrow-derived stromal cell line. After these seminal findings, accumulating data indicated RANKL and RANK not only as essential players for the development and activation of osteoclasts, but also for the correct differentiation of medullary thymic epithelial cells (mTECs) that act as mediators of the central tolerance process by which self-reactive T cells are eliminated while regulatory T cells are generated. In light of the RANKL-RANK multi-task function, an antibody targeting this pathway, denosumab, is now commonly used in the therapy of bone loss diseases including chronic inflammatory bone disorders and osteolytic bone metastases; furthermore, preclinical data support the therapeutic application of denosumab in the framework of a broader spectrum of tumors. Here, we discuss advances in cellular and molecular mechanisms elicited by RANKL-RANK pathway in the bone and thymus, and the extent to which its inhibition or augmentation can be translated in the clinical arena.

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“…The results indicated that the strontium ion release could hinder the osteoclastogenesis which was consistent with previous studies. 23,[47][48][49]…”

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confidence: 99%

<p>The Fabrication and Function of Strontium-modified Hierarchical Micro/Nano Titanium Implant</p>

Wang

et al. 2020

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The induction of RANKL molecule clustering could stimulate early osteoblast differentiation

Cited by 18 publications

References 25 publications

Resveratrol promotes osteoblastic differentiation in a rat model of postmenopausal osteoporosis by regulating autophagy

Resveratrol promotes osteoblastic differentiation in a rat model of postmenopausal osteoporosis by regulating autophagy

The RANKL-RANK Axis: A Bone to Thymus Round Trip

<p>The Fabrication and Function of Strontium-modified Hierarchical Micro/Nano Titanium Implant</p>

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