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白细胞介素-1β诱导环氧化酶-2 的表达,促进卵巢子宫内膜异位症来源的人间质干细胞的侵袭能力。

Interleukin-1β induces cyclooxygenase-2 expression and promotes the invasive ability of human mesenchymal stem cells derived from ovarian endometrioma.

机构信息

Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan.

出版信息

Fertil Steril. 2011 Sep;96(3):678-684.e1. doi: 10.1016/j.fertnstert.2011.06.041. Epub 2011 Jul 16.

Abstract

OBJECTIVE

To elucidate the role of interleukin-1β (IL-1β) on cyclooxygenase-2 (COX-2) expression and invasion of endometrioma-derived ectopic endometrial mesenchymal stem cells (EN-MSCs) and to develop an organoid method to study the invasive ability of endometrial cells.

DESIGN

Gene expression and cell functions.

SETTING

Kaohsiung Medical University, Kaohsiung, Taiwan.

PATIENT(S): Human eutopic and endometrioma-derived ectopic EN-MSCs were isolated from different endometrium biopsy samples after surgery for treatment of endometriosis.

INTERVENTION(S): Chemical treatment of cell culture.

MAIN OUTCOME MEASURE(S): Comparative analysis of genomewide messenger RNA (mRNA) expression, cell migration, and invasion abilities in cell culture and organoid culture.

RESULT(S): Gene expression profiles revealed that the expression of IL-1β and COX-2 were statistically significantly higher in ectopic EN-MSCs compared with eutopic EN-MSCs. These enhanced expressions coincided with a greater ability for cell migration and invasion in ectopic EN-MSCs and were found to be distinctly regulated by IL-1β which up-regulates COX-2 expression. Furthermore, IL-1β treatment of ectopic EN-MSCs in organoids was found to induce tentacle-like structures that mimicked cell invasion.

CONCLUSION(S): These results indicate that COX-2 and IL-1β regulate the invasion ability of ectopic EN-MSCs. The information may be useful for developing a new therapeutic strategy for endometriosis. The ex vivo invasion model will be useful for characterization of EN-MSCs.

摘要

目的

阐明白细胞介素-1β(IL-1β)在环氧合酶-2(COX-2)表达和子宫内膜异位症来源的异位子宫内膜间充质干细胞(EN-MSCs)侵袭中的作用,并开发一种类器官方法来研究子宫内膜细胞的侵袭能力。

设计

基因表达和细胞功能。

地点

台湾高雄医科大学。

患者

人正常子宫内膜和子宫内膜异位症来源的异位 EN-MSCs 是从不同子宫内膜活检样本中分离出来的,这些样本是在子宫内膜异位症治疗手术后获得的。

干预

细胞培养的化学处理。

主要观察指标

细胞培养和类器官培养中基因组信使 RNA(mRNA)表达、细胞迁移和侵袭能力的比较分析。

结果

基因表达谱显示,与正常子宫内膜来源的 EN-MSCs 相比,异位 EN-MSCs 中 IL-1β 和 COX-2 的表达明显更高。这些增强的表达与异位 EN-MSCs 中更强的细胞迁移和侵袭能力一致,并且发现 IL-1β 明显调节 COX-2 的表达。此外,在类器官中用 IL-1β 处理异位 EN-MSCs 被发现诱导出类似细胞侵袭的触手样结构。

结论

这些结果表明 COX-2 和 IL-1β 调节异位 EN-MSCs 的侵袭能力。这些信息可能有助于为子宫内膜异位症开发新的治疗策略。该体外侵袭模型将有助于 EN-MSCs 的特征描述。

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