骨愈合
细胞生物学
MAPK/ERK通路
树突状细胞
骨细胞
免疫抑制
炎症
化学
癌症研究
信号转导
免疫系统
机制(生物学)
转录因子
细胞
骨吸收
PI3K/AKT/mTOR通路
骨免疫学
成骨细胞
移植
再生(生物学)
蛋白激酶B
骨形成
间充质干细胞
细胞信号
骨重建
作者
Yuya Dai,Jinhui Wu,Junyou Wang,Haoze Wang,Bingqing Guo,Tao Jiang,Zhuyun Cai,Junjie Han,Haoyu Zhang,Bangzhe Xu,Xuhui Zhou,Ce Wang
出处
期刊:Small
[Wiley]
日期:2024-04-25
卷期号:20 (33): e2311344-e2311344
被引量:16
标识
DOI:10.1002/smll.202311344
摘要
Abstract The effect of immunoinflammation on bone repair during the recovery process of bone defects needs to be further explored. It is reported that Mg 2+ can promote bone repair with immunoregulatory effect, but the underlying mechanism on adaptive immunity is still unclear. Here, by using chitosan and hyaluronic acid‐coated Mg 2+ (CSHA‐Mg) in bone‐deficient mice, it is shown that Mg 2+ can inhibit the activation of CD4 + T cells and increase regulatory T cell formation by inducing immunosuppressive dendritic cells (imDCs). Mechanistically, Mg 2+ initiates the activation of the MAPK signaling pathway through TRPM7 channels on DCs. This process subsequently induces the downstream HIF‐1α expression, a transcription factor that amplifies TGF‐β production and inhibits the effective T cell function. In vivo, knock‐out of HIF‐1α in DCs or using a HIF‐1α inhibitor PX‐478 reverses inhibition of bone inflammation and repair promotion upon Mg 2+ ‐treatment. Moreover, roxadustat, which stabilizes HIF‐1α protein expression, can significantly promote immunosuppression and bone repair in synergism with CSHA‐Mg. Thus, the findings identify a key mechanism for DCs and its HIF‐1α‐TGF‐β axis in the induction of immunosuppressive bone microenvironment, providing potential targets for bone regeneration.
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