Osteoclast stimulatory transmembrane protein induces a phenotypic switch in macrophage polarization suppressing an M1 pro-inflammatory state

Osteoclast stimulatory transmembrane protein induces a phenotypic switch in macrophage polarization suppressing an M1 pro-inflammatory state
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破骨细胞刺激跨膜蛋白诱导巨噬细胞极化表型转换,抑制 M1 促炎状态

DOI:
10.1093/abbs/gmx092
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发表时间:
2017-10-01
影响因子:
3.7
通讯作者:
Chen, Fengling
Chen, Fengling
中科院分区:
生物学3区
文献类型:
--
作者:
Yuan, Huimin;He, Jiangping;Chen, Fengling

文献摘要

被引文献

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巨噬细胞是代谢综合征的关键细胞,也是代谢性疾病的危险因素。巨噬细胞具有不同的功能和转录谱,但都是维持体内平衡所必需的。众所周知,巨噬细胞在炎症和早期动脉粥样硬化形成中起关键作用,并且存在两种表型:促炎(M1)和抗炎(M2)。破骨细胞刺激跨膜蛋白(oc-stamp)是一种多通道跨膜蛋白,但其功能尚不清楚。在这项研究中,我们探讨了oc-stamp在巨噬细胞生理学中的作用。结果表明,LPS和IFN-γ刺激后,α-stamp明显降低,IL-4刺激后,α-stamp明显升高。此外,oc-stamp诱导巨噬细胞极化的表型转换,抑制过表达组中的M1促炎状态,并促进敲除组中的M1促炎状态。进一步的研究表明,α-stamp可能通过STAT 6调节巨噬细胞的极化。综上所述,我们的结果首次证明了α-stamp可能在巨噬细胞极化中发挥重要作用并抑制M1促炎状态。
Macrophages are the key cells in metabolic syndrome and are also a risk factor for metabolic disease. Macrophages have different functions and transcriptional profiles, but all are required for maintaining homeostasis. It is well known that macrophages play a key role in inflammation and early atherogenesis, and are present in two phenotypes: pro-inflammatory (M1) and anti-inflammatory (M2). Osteoclast stimulatory transmembrane protein (oc-stamp) is a multiple-pass transmembrane protein; however, its function remains unclear. In this study, we explored the role of oc-stamp in macrophages physiology. The results showed that oc-stamp was notably decreased under LPS and IFN-γ stimulation, while it was increased with IL-4 treatment. Furthermore, oc-stamp induced a phenotypic switch in macrophage polarization, suppressing the M1 pro-inflammatory state in the overexpression group, and promoting the M1 pro-inflammatory state in the knockdown group. Further study revealed that oc-stamp regulated macrophage polarization possibly via STAT6. Taken together, our results are the first to demonstrate that oc-stamp may play an important role in macrophage polarization and inhibit the M1 pro-inflammatory state.