2021年7月
Dectin-1–mediated suppression of RANKL-induced osteoclastogenesis by glucan from baker's yeast
Journal of Cellular Physiology
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- 巻
- 236
- 号
- 7
- 開始ページ
- 5098
- 終了ページ
- 5107
- 記述言語
- 掲載種別
- 研究論文(学術雑誌)
- DOI
- 10.1002/jcp.30217
Immunoreceptors expressed on osteoclast precursor cells modify osteoclast differentiation and bone resorption activity. Dectin-1 is a lectin receptor of β-glucan and is specifically expressed in osteoclast precursor cells. In this study, we evaluated the bioactivity of β-glucan on receptor activator of nuclear factor-kappa B ligand (RANKL)-induced osteoclastogenesis and observed that glucan from baker's yeast inhibited this process in mouse bone marrow cells and dectin-1–overexpressing RAW264.7 (d-RAW) cells. In conjunction, RANKL-induced nuclear factor of activated T cell c1 expression was suppressed, subsequently downregulating TRAP and Oc-stamp. Additionally, nuclear factor-kappa B activation and the expression of c-fos and Blimp1 were reduced in d-RAW cells. Furthermore, glucan from baker's yeast induced the degradation of Syk protein, essential factor for osteoclastogenesis. These results suggest that glucan from baker's yeast suppresses RANKL-induced osteoclastogenesis and can be applied as a new treatment strategy for bone-related diseases.
- リンク情報
- ID情報
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- DOI : 10.1002/jcp.30217
- ISSN : 0021-9541
- eISSN : 1097-4652
- ORCIDのPut Code : 87430366
- PubMed ID : 33305824
- SCOPUS ID : 85097414243