GRIM-19在子宫腺肌病中的表达及促进疾病发展的机制研究

发布时间：2018-10-11 10:07

【摘要】：目的研究诱导细胞凋亡相关基因-19(GRIM-19)在子宫腺肌病患者子宫内膜组织中的表达水平,并探讨其在疾病发生发展中的分子机制。方法取30例子宫腺肌病患者异位和在位内膜组织,采用免疫组织化学和Western blot检测内膜组织中GRIM-19、磷酸化信号转导及转录激活蛋白3(pSTAT3)和内皮生长因子(VEGF)的表达水平。采用TUNEL检测内膜组织凋亡,CD34抗体直接检测内膜组织新生血管形成。构建GRIM-19siRNA和重组质粒,转染Ishikawa细胞后检测下游信号分子pSTAT3、信号转导和转录激活因子3(STAT3)和VEGF的变化。结果与对照组相比,子宫腺肌病患者在位内膜和异位内膜组织中GRIM-19表达水平降低。在位内膜和异位内膜组织中细胞凋亡减少,微血管密度、pSTAT3和VEGF表达水平升高。转染Ishikawa细胞,下调GRIM-19表达可显著激活pSTAT3和VEGF。结论 GRIM-19通过抑制细胞凋亡和增加新生血管形成,促进子宫腺肌病的发生发展。
[Abstract]:Objective to investigate the expression of apoptosis-related gene-19 (GRIM-19) in endometrial tissues of patients with adenomyosis and to explore its molecular mechanism in the pathogenesis of adenomyosis. Methods the expression of GRIM-19, phosphorylation signal transduction and transcription activator protein 3 (pSTAT3) and endothelial growth factor (VEGF) were detected by immunohistochemistry and Western blot in 30 cases of ectopic and eutopic endometrium of adenomyosis. Tunica intima apoptosis was detected by TUNEL and neovascularization was detected by CD34 antibody. GRIM-19siRNA and recombinant plasmid were constructed and transfected into Ishikawa cells to detect the changes of pSTAT3, signal transduction and transcription activator 3 (STAT3) and VEGF. Results compared with the control group, the expression of GRIM-19 in eutopic endometrium and ectopic endometrium was decreased in patients with adenomyosis. Apoptosis decreased, microvessel density, pSTAT3 and VEGF expression increased in eutopic and ectopic endometrium. Transfection of Ishikawa cells, down-regulation of GRIM-19 expression can significantly activate pSTAT3 and VEGF. Conclusion GRIM-19 can promote the development of adenomyosis by inhibiting apoptosis and increasing neovascularization.
【作者单位】：川北医学院附属医院妇产科;
【分类号】：R711.71

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