肿瘤坏死因子α基因沉默降低了脂多糖促进的子宫内膜异位症间质细胞增殖。
TNFalpha gene silencing reduced lipopolysaccharide-promoted proliferation of endometriotic stromal cells.
作者信息
Miyamoto Ayako, Taniguchi Fuminori, Tagashira Yukiko, Watanabe Ayako, Harada Tasuku, Terakawa Naoki
机构信息
Department of Obstetrics and Gynecology, Tottori University School of Medicine, Nishimachi, Yonago, Japan.
出版信息
Am J Reprod Immunol. 2009 Apr;61(4):277-85. doi: 10.1111/j.1600-0897.2009.00691.x.
PROBLEM
We previously reported that lipopolysaccharide (LPS)-promoted endometriotic stromal cell (ESC) proliferation by inducing TNFalpha production. The aim of this study was to investigate the efficacy of TNFalpha gene silencing on LPS-treated ESCs.
METHOD OF STUDY
Endometriotic stromal cells (ESCs) and endometrial stromal cells (ESCs) (EMSCs) were obtained from ovarian chocolate cysts and uterine myoma, respectively. Using PCR array, LPS-induced gene expression profiling after transfection of TNFalpha siRNA into ESCs was performed. Down-regulated genes by TNFalpha silencing were examined using real-time RT-PCR. Effect of TNFalpha silencing was examined using ELISA and BrdU incorporation, respectively.
RESULTS
In PCR array, TNFalpha silencing in ESCs repressed LPS-induced expression of cIAP2 and IL-8, NFkappaB pathway responsive genes. After adding LPS, the levels of cIAP2 and IL-8 expression in ESCs were higher compared with those in EMSCs. TNFalpha silencing attenuated the LPS-induced ESC proliferation.
CONCLUSION
Tumor necrosis factor alpha may be involved in cell proliferation of endometriotic tissues.
问题
我们之前报道过，脂多糖（LPS）通过诱导肿瘤坏死因子α（TNFα）的产生促进子宫内膜异位症间质细胞（ESC）增殖。本研究的目的是探讨TNFα基因沉默对LPS处理的ESC的影响。
研究方法
分别从卵巢巧克力囊肿和子宫肌瘤中获取子宫内膜异位症间质细胞（ESC）和子宫内膜间质细胞（EMSC）。利用PCR阵列技术，对转染TNFα siRNA后的ESC进行LPS诱导的基因表达谱分析。采用实时RT-PCR检测TNFα沉默后下调的基因。分别用ELISA和BrdU掺入法检测TNFα沉默的效果。
结果
在PCR阵列中，ESC中的TNFα沉默抑制了LPS诱导的细胞凋亡抑制蛋白2（cIAP2）和白细胞介素8（IL-8）的表达，这两种基因是核因子κB（NFκB）信号通路的反应基因。添加LPS后，ESC中cIAP2和IL-8的表达水平高于EMSC。TNFα沉默减弱了LPS诱导的ESC增殖。
结论
肿瘤坏死因子α可能参与子宫内膜异位组织的细胞增殖。
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