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目的探讨早孕滋养层细胞有节制地侵入机制,研究肿瘤坏死因子α(TNFα)诱导滋养层细胞基质金属蛋白酶9(MMP9)基因表达的调控机制。方法2004年南方医科大学南方医院将10-4g/LTNFα分别处理滋养层细胞0、5、10、20、30min后,应用细胞ELISA法测定滋养层细胞中蛋白激酶的活性变化;预先给予丝裂原活化蛋白激酶(MAPK)的特异性抑制剂处理滋养层细胞30min,然后给予10-4g/LTNFα处理滋养层细胞24h,应用反转录聚合酶链反应(RTPCR)检测滋养层细胞MMP9基因表达的变化。结果发现10-4g/LTNFα均能迅速激活滋养层细胞的细胞外信号调节蛋白激酶(ERK)、cjun氨基末端激酶(JNK)、p38MAPK激酶活性。TNFα刺激滋养层细胞引起MMP9mRNA表达显著增加,其能被ERK或p38MAPK的特异性抑制剂所抑制。结论ERK和p38MAPK可能是TNFα诱导滋养层细胞MMP9基因表达增加的重要调节物质。
OBJECTIVE: To investigate the regulatory mechanism of trophoblast cells in the first trimester of pregnancy in order to study the mechanism of tumor necrosis factor-α (TNFα) -induced matrix metalloproteinase-9 (MMP9) gene expression. Methods Southern Hospital of Southern Medical University in 2004, 10-4g / LTNFα were treated trophoblast cells 0,5,10,20,30 min, the application of cell ELISA assay of trophoblast cell protein kinase activity changes; pre-given mitogen Trophoblast cells were treated with specific inhibitor of activated protein kinase (MAPK) for 30 min and then treated with 10-4 g / LTNFα for 24 h. RT-PCR was used to detect the changes of MMP9 gene expression in trophoblastic cells . The results showed that 10-4g / LTNFα could rapidly activate extracellular signal-regulated protein kinase (ERK), cjun aminotubermin (JNK) and p38MAPK kinase in trophoblast cells. TNFα stimulation of trophoblast cells causes a significant increase in MMP9 mRNA expression, which can be inhibited by specific inhibitors of ERK or p38MAPK. Conclusion ERK and p38MAPK may be important mediators of TNFα-induced MMP9 gene expression in trophoblast cells.