Sommer Grit, Weise Sebastian, Kralisch Susan, Scherer Philipp E, Lössner Ulrike, Blüher Matthias, Stumvoll Michael, Fasshauer Mathias
Department of Internal Medicine III, University of Leipzig, 04103 Leipzig, Germany.
J Cell Biochem. 2008 Aug 15;104(6):2241-7. doi: 10.1002/jcb.21782.
Serum amyloid A (SAA) 3 has been characterized as an inflammatory adipocyte-secreted acute-phase reactant. In the current study, regulation of SAA3 by the proinflammatory and insulin resistance-inducing cytokine interleukin (IL)-1beta was determined in 3T3-L1 and brown adipocytes. Interestingly, SAA3 mRNA and protein synthesis were dramatically increased by IL-1beta in a time-dependent fashion with maximal induction after 24 h. Furthermore, IL-1beta significantly induced SAA3 mRNA expression dose-dependently with maximal 36.4-fold upregulation seen at 2 ng/ml effector. Moreover, IL-1beta-induced SAA3 expression was mediated by nuclear factor-kappaB and janus kinase 2. Taken together, our data show a potent upregulation of SAA3 by IL-1beta.
血清淀粉样蛋白A(SAA)3已被鉴定为一种由炎症性脂肪细胞分泌的急性期反应物。在本研究中,我们在3T3-L1细胞和棕色脂肪细胞中确定了促炎和诱导胰岛素抵抗的细胞因子白细胞介素(IL)-1β对SAA3的调控作用。有趣的是,IL-1β能以时间依赖性方式显著增加SAA3的mRNA和蛋白质合成,在24小时后诱导作用达到最大值。此外,IL-1β能显著地剂量依赖性诱导SAA3 mRNA表达,在效应物浓度为2 ng/ml时上调幅度最大,可达36.4倍。而且,IL-1β诱导的SAA3表达是由核因子-κB和janus激酶2介导的。综上所述,我们的数据表明IL-1β能强力上调SAA3。