AdipoR1通过FUNDC1调节线粒体功能,促进致病性Th17分化。

IF 2.2 4区 医学 Q3 MEDICINE, RESEARCH & EXPERIMENTAL Journal of Biomedical Research Pub Date : 2024-11-25 DOI:10.7555/JBR.38.20240244
Hui Wang, Qian Zhang, Yuankai Sun, Wenfeng Tan, Miaojia Zhang
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引用次数: 0

摘要

研究表明,脂肪连接素受体1(Adipor1)缺乏可抑制Th17细胞分化,减少抗原诱导的关节炎(AIA)小鼠的关节炎症和骨侵蚀。新出现的证据表明,Th17 细胞可分化为致病性细胞(pTh17)和非致病性细胞(npTh17),其中 pTh17 细胞在多种自身免疫和炎症中发挥着关键作用。在目前的研究中,我们发现 Adipor1 的缺乏会抑制 pTh17 在体外的分化,而且在 pTh17 细胞中缺失 Adipor1 会降低线粒体功能。RNA测序(RNA-seq)表明,在Adipor1缺陷的CD4 + T细胞中,与线粒体功能相关的基因Fundc1的表达水平显著增加。在Adipor1缺陷的CD4 + T细胞中干扰Fundc1的表达部分缓解了Adipor1缺陷对线粒体功能和pTh17分化的影响。总之,本研究证明了 AdipoR1 在通过 FUNDC1 调节线粒体功能以促进 pTh17 细胞分化方面的新作用,为自身免疫性疾病和炎症性疾病的潜在治疗靶点提供了一些启示。
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AdipoR1 promotes pathogenic Th17 differentiation by regulating mitochondrial function through FUNDC1.

Adiponectin receptor 1 ( Adipor1) deficiency has been shown to inhibit Th17 cell differentiation and reduce joint inflammation and bone erosion in antigen-induced arthritis (AIA) mice. Additional emerging evidence indicates that Th17 cells may differentiate into pathogenic (pTh17) and non-pathogenic (npTh17) cells, with the pTh17 cells playing a crucial role in numerous autoimmune and inflammatory conditions. In the current study, we found that Adipor1 deficiency inhibited pTh17 differentiation in vitro and that the deletion of Adipor1 in pTh17 cells reduced the mitochondrial function. RNA-sequencing (RNA-seq) demonstrated a significant increase in the expression levels of Fundc1, a gene related to mitochondrial function, in Adipor1-deficient CD4 + T cells. Interference with the Fundc1 expression in Adipor1-deficient CD4 + T cells partially mitigated the effect of Adipor1 deficiency on mitochondrial function and pTh17 differentiation. In conclusion, the current study demonstrated a novel role of AdipoR1 in regulating mitochondrial function via FUNDC1 to promote pTh17 cell differentiation, providing some insights into potential therapeutic targets for autoimmune and inflammatory diseases.

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来源期刊
Journal of Biomedical Research
Journal of Biomedical Research MEDICINE, RESEARCH & EXPERIMENTAL-
CiteScore
4.60
自引率
0.00%
发文量
69
期刊最新文献
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