Combination of 17β-estradiol with the environmental pollutant TCDD is involved in pathogenesis of endometriosis via up-regulating the chemokine I-309-CCR8
Combination of 17β-estradiol with the environmental pollutant TCDD is involved in pathogenesis of endometriosis via up-regulating the chemokine I-309-CCR8
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DOI：
10.1016/j.fertnstert.2006.11.129
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发表时间：
2007-08-01
影响因子：
6.7
通讯作者：
Li, Da-Jin
中科院分区：
文献类型：
--
作者：
Shi, Ying-Li;Luo, Xue-Zhen;Li, Da-Jin
目的：探讨E-2与环境污染物2,3,7,8-四氯二苯并二恶英（TCDD）联用对子宫内膜异位症发病机制中子宫内膜异位病灶相关细胞CCR8-I-309表达的影响。设计：前瞻性实验室研究。地点：大学医院。患者：中国子宫内膜异位症女性。干预：子宫内膜异位组织和匹配的子宫内膜异位症患者。收集在位子宫内膜。子宫内膜基质细胞 (ESC)、HPMC 和 U937 细胞用 17 beta-E-2 或 TCDD 处理。用I-309刺激ESC。 主要指标(S)：通过逆转录聚合酶链反应和免疫组化分析组织中CCR8的表达。通过流式细胞术分析I-309对整合素β1和αvβ03表达强度的影响，并通过趋化实验探讨I-309对ESC的趋化活性。通过酶联免疫吸附测定对培养物上清液中I-309的浓度进行定量。结果：CCR8在子宫内膜异位组织中过表达。 I-309 促进整合素 β1 的表达。雌二醇和 TCDD 上调 ESC 的 CCR8 表达。雌二醇放大了 TCDD 对 U937 分泌 I-309 的刺激作用。 HPMC和U937细胞的相互作用促进了I-309的分泌。结论：这些发现表明17β-E-2与环境污染物TCDD的结合通过上调趋化因子CCR8-I-309参与子宫内膜异位症的发病机制。
Objective: To explore the effects of the combined E-2 with the environmental pollutant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on CCR8-I-309 expression by the endometriotic lesion-associated cells in the pathogenesis of endometriosis.Design: Prospective laboratory study.Setting: University hospital.Patient(s): Chinese women with endometriosis.Intervention(s): The endometriotic tissue and matched eutopic endometrium were collected. Endometrial stromal cells (ESCs), HPMC, and U937 cells were treated with 17 beta-E-2 or TCDD. The ESCs were stimulated with I-309.Main Outcome Measure(S): The expression of CCR8 in tissues was analyzed by reverse transcription-polymerase chain reaction and immunohistochemistry. The effect of I-309 on integrin beta 1 and alpha v beta 03 expression intensity was analyzed by flow cytometry, and the chemotactic activity of I-309 on the ESC was explored by chemotactic assay. Concentration of I-309 in the culture supernatant was quantified by enzyme-linked immumosorbent assay.Result(s): CCR8 was overexpressed in the endometriotic tissue. I-309 promoted the expression of integrin beta 1. Estradiol and TCDD up-regulated CCR8 expression by ESCs. Estradiol magnified the stimulatory effect of TCDD on I-309 secretion by U937. The interaction of HPMC and U937 cells promoted I-309 secretion.Conclusion(s): These findings imply that the combination of 17 beta-E-2 with the environmental pollutant TCDD is involved in the pathogenesis of endometriosis via up-regulating the chemokine CCR8 -I-309.