Dectin-1-mediated suppression of RANKL-induced osteoclastogenesis by glucan from baker's yeast
Dectin-1-mediated suppression of RANKL-induced osteoclastogenesis by glucan from baker's yeast
复制标题
Dectin-1 介导的面包酵母葡聚糖抑制 RANKL 诱导的破骨细胞生成
DOI：
10.1002/jcp.30217
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发表时间：
2021
期刊：
影响因子：
5.6
通讯作者：
Wataru Ariyoshi
中科院分区：
文献类型：
--
作者：
Shiika Hara;Yoshie Nagai-Yoshioka;Ryota Yamasaki;Yoshiyuki Adachi;Yuko Fujita;Kouji Watanabe;Kenshi Maki;Tatsuji Nishihara;Wataru Ariyoshi
破骨细胞前体细胞上表达的免疫受体改变破骨细胞分化和骨吸收活性。Dectin-1是β-葡聚糖的凝集素受体，在破骨细胞前体细胞中特异性表达。在这项研究中，我们评估了β-葡聚糖对核因子-κ B配体受体激活剂（RANKL）诱导的破骨细胞生成的生物活性，并观察到面包酵母葡聚糖抑制小鼠骨髓细胞和dectin-1过表达RAW 264. 7（d-RAW）细胞中的这一过程。同时，RANKL诱导的活化T细胞核因子c1表达受到抑制，随后下调TRAP和Oc‐stamp。此外，核因子-κ B活化以及c-fos和Blimp 1的表达在d-RAW细胞中减少。此外，面包酵母的葡聚糖诱导破骨细胞生成的必需因子Syk蛋白的降解。这些结果表明，来自面包酵母的葡聚糖可抑制RANKL诱导的破骨细胞生成，可作为骨相关疾病的新治疗策略。
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.