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激活素A对小鼠腹腔巨噬细胞活性的影响。

Effects of activin A on the activities of the mouse peritoneal macrophages.

作者信息

Zhang Xue Jun, Li Yang, Tai Gui Xiang, Xu Gui Yue, Zhang Peng Yu, Yang Yu, Lao Feng Xue, Liu Zhong Hui

机构信息

Department of Immunology, School of Basic Medical Sciences, Jilin University, Changchun, China.

出版信息

Cell Mol Immunol. 2005 Feb;2(1):63-7.

PMID:16212913
Abstract

Activin A is a kind of pre-inflammatory factor that belongs to the transforming growth factor-beta (TGF-beta) superfamily. To investigate the effect and mechanism of activin A on the activities of mouse macrophages, the secretion of NO in the supernatant of cultured mouse peritoneal macrophages was examined by NO assay kit, and the expression of iNOS, ActRIIA and ARIP2 mRNA in mouse peritoneal macrophages was analyzed by RT-PCR. The results showed that activin A stimulated the secretion of NO and the expression of iNOS mRNA in non-activated mouse macrophages in a time- and dose-dependent manner. In contrast, activin A in the same concentration inhibited the secretion of NO in LPS-activated mouse macrophages in a dose-dependent manner. ActRIIA was highly expressed on macrophages, and activin A upregulated the ActRIIA mRNA expression in macrophages. Anti-ActRIIA antibody can block the secretion of NO from the macrophages stimulated by activin A. Furthermore, RT-PCR analysis revealed that activin A enhanced the ARIP2 mRNA expression in macrophages. These results indicated that Activin A may be a weak activator compared with LPS to mouse macrophages, and activin A may modulate the secretion of NO through ActRIIA-ARIP2 signal pathway in mouse macrophages.

摘要

激活素A是一种属于转化生长因子-β(TGF-β)超家族的促炎前因子。为了研究激活素A对小鼠巨噬细胞活性的影响及其机制,采用NO检测试剂盒检测培养的小鼠腹腔巨噬细胞上清液中NO的分泌情况,并用RT-PCR分析小鼠腹腔巨噬细胞中诱导型一氧化氮合酶(iNOS)、激活素受体IIA(ActRIIA)和激活素受体相互作用蛋白2(ARIP2)mRNA的表达。结果表明,激活素A能以时间和剂量依赖性方式刺激未激活的小鼠巨噬细胞分泌NO及iNOS mRNA的表达。相反,相同浓度的激活素A能以剂量依赖性方式抑制脂多糖(LPS)激活的小鼠巨噬细胞分泌NO。ActRIIA在巨噬细胞上高表达,激活素A能上调巨噬细胞中ActRIIA mRNA的表达。抗ActRIIA抗体可阻断激活素A刺激巨噬细胞分泌NO。此外,RT-PCR分析显示激活素A能增强巨噬细胞中ARIP2 mRNA的表达。这些结果表明,与LPS相比,激活素A对小鼠巨噬细胞可能是一种较弱的激活剂,且激活素A可能通过ActRIIA-ARIP2信号通路调节小鼠巨噬细胞中NO的分泌。

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