Department of Immunology, College of Basic Medical Sciences, Jilin University, Changchun, China.
Department of Genetics, College of Basic Medical Sciences, Jilin University, Changchun, China.
Sci Rep. 2017 Sep 4;7(1):10306. doi: 10.1038/s41598-017-10855-4.
The bacterial endotoxin lipopolysaccharide (LPS), a key pathogenic stimulator, can induce the activation of macrophages. Activin receptor-interacting protein 2 (ARIP2), an intracellular signaling protein, has a wide histological distribution, however, whether ARIP2 is involved in regulation of activation of macrophages was not well characterized. Here, by immunocytochemical staining, we found that ARIP2 protein existed in monocyte-macrophage cell line RAW264.7 cells and peritoneal macrophages of mouse, and ARIP2 expression in RAW264.7 cells was up-regulated by LPS. Furthermore, the results revealed that ARIP2 overexpression in the LPS-activated RAW264.7 cells inhibited the productions of IL-1β and TNFα, phagocytic activities and CD14 expression, whereas did not alter expressions of MyD88, TLR2 and TLR4. Additionally, in vivo ARIP2 overexpression also reduced the productions of IL-1β and TNFα from the LPS-stimulated peritoneal macrophages of mouse. These data suggest that ARIP2 may play an anti-inflammatory role in macrophages via inhibiting CD14 expression.
细菌内毒素脂多糖 (LPS) 作为一种关键的致病刺激物，可诱导巨噬细胞的激活。激活素受体相互作用蛋白 2 (ARIP2) 是一种细胞内信号蛋白，具有广泛的组织学分布，然而，ARIP2 是否参与调节巨噬细胞的激活尚未得到很好的描述。在这里，通过免疫细胞化学染色，我们发现 ARIP2 蛋白存在于单核巨噬细胞系 RAW264.7 细胞和小鼠腹腔巨噬细胞中，LPS 可上调 RAW264.7 细胞中的 ARIP2 表达。此外，结果表明，LPS 激活的 RAW264.7 细胞中过表达 ARIP2 可抑制 IL-1β 和 TNFα 的产生、吞噬活性和 CD14 表达，而不改变 MyD88、TLR2 和 TLR4 的表达。此外，体内过表达 ARIP2 也可降低 LPS 刺激的小鼠腹腔巨噬细胞中 IL-1β 和 TNFα 的产生。这些数据表明，ARIP2 可能通过抑制 CD14 表达在巨噬细胞中发挥抗炎作用。
