Taurine chloramine differentially inhibits matrix metalloproteinase 1 and 13 synthesis in interleukin-1beta stimulated fibroblast-like synoviocytes.
Taurine chloramine differentially inhibits matrix metalloproteinase 1 and 13 synthesis in interleukin-1beta stimulated fibroblast-like synoviocytes.
复制标题
牛磺酸氯胺差异抑制了白介素-1beta中的基质金属蛋白酶1和13合成刺激的成纤维细胞样细胞。
DOI：
10.1186/ar2279
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发表时间：
2007
影响因子：
4.9
通讯作者：
Yoo, Myung Chul
中科院分区：
文献类型：
--
作者：
Kim, Kyoung Soo;Park, Eun Kyung;Ju, Seung Min;Jung, Hye-Sook;Bang, Jun Soo;Kim, Chaekyun;Lee, Yeon-Ah;Hong, Seung-Jae;Lee, Sang-Hoon;Yang, Hyung-In;Yoo, Myung Chul
有研究表明，牛磺酸氯胺（TauCl）在下调促炎介质中起重要作用。然而，其对基质金属蛋白酶（MMPs）表达的影响尚不清楚。在本研究中，我们研究了TauCl对MMPs滑膜表达的影响。采用以下方法研究了TauCl对IL-1β刺激的成纤维细胞样滑膜细胞（FLSs）中MMP表达的影响。采用实时荧光定量PCR和半定量PCR分析MMPs mRNA的表达情况。ELISA法检测MMPs蛋白水平。Western blot分析丝裂原活化蛋白激酶和核因子-κB激酶抑制剂信号通路。最后，采用电泳迁移量转移法和免疫组织化学方法评估转录因子的定位。IL-1β增加类风湿关节炎FLSs中MMP-1和MMP-13的转录和翻译水平，而MMP-2和MMP-9的水平不受影响。400 ~ 600 μmol/l的TauCl显著抑制了MMP-13的转录和翻译表达，而800 μmol/l的TauCl则显著抑制了MMP-1的表达。在600 μmol/l浓度下，TauCl对IL-1β刺激的类风湿关节炎FLSs中丝裂原活化蛋白激酶磷酸化和i - κ b降解无显著抑制作用。当TauCl浓度为800 μmol/l时，i - κ b的降解被显著抑制。电泳迁移量转移法和核因子-κB定位免疫化学染色证实了TauCl对i -κB降解的抑制作用。TauCl对MMP-1和MMP-13的表达有不同的抑制作用，主要通过抑制i - κ b降解来抑制MMP-1的表达，而通过i - κ b途径以外的信号通路抑制MMP-13的表达。
It has been suggested that taurine chloramine (TauCl) plays an important role in the downregulation of proinflammatory mediators. However, little is known about its effect on the expression of matrix metalloproteinases (MMPs). In this study, we investigated the effects of TauCl on synovial expression of MMPs. The effects of TauCl on MMP expression in IL-1β stimulated fibroblast-like synoviocytes (FLSs) were studied using the following techniques. Real-time PCR and semi-quantitative PCR were employed to analyze the mRNA expression of MMPs. ELISA was used to determine protein levels of MMPs. Western blot analyses were performed to analyze the mitogen-activated protein kinase and inhibitor of nuclear factor-κB (IκB) kinase signalling pathways. Finally, electrophoretic mobility shift assay and immunohistochemistry were used to assess localization of transcription factors. IL-1β increased the transcriptional and translational levels of MMP-1 and MMP-13 in rheumatoid arthritis FLSs, whereas the levels of MMP-2 and MMP-9 were unaffected. TauCl at a concentration of 400 to 600 μmol/l greatly inhibited the transcriptional and translational expression of MMP-13, but the expression of MMP-1 was significantly inhibited at 800 μmol/l. At a concentration of 600 μmol/l, TauCl did not significantly inhibit phosphorylation of mitogen-activated protein kinase or IκB degradation in IL-1β stimulated rheumatoid arthritis FLSs. The degradation of IκB was significantly inhibited at a TauCl concentration of 800 μmol/l. The inhibitory effect of TauCl on IκB degradation was confirmed by electrophoretic mobility shift assay and immunochemical staining for localization of nuclear factor-κB. TauCl differentially inhibits the expression of MMP-1 and MMP-13, and inhibits expression of MMP-1 primarily through the inhibition of IκB degradation, whereas it inhibits expression of MMP-13 through signalling pathways other than the IκB pathway.