Ying-Li Shi1, Xue-Zhen Luo, Xiao-Yong Zhu, Da-Jin Li. 1. Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, China.
Abstract
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 17beta-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 beta1 and alphavbeta3 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 immunosorbent assay. RESULT(S): CCR8 was overexpressed in the endometriotic tissue. I-309 promoted the expression of integrin beta1. 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 17beta-E(2) with the environmental pollutant TCDD is involved in the pathogenesis of endometriosis via up-regulating the chemokine CCR8-I-309.
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 17beta-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 beta1 and alphavbeta3 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 immunosorbent assay. RESULT(S): CCR8 was overexpressed in the endometriotic tissue. I-309 promoted the expression of integrin beta1. 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 17beta-E(2) with the environmental pollutant TCDD is involved in the pathogenesis of endometriosis via up-regulating the chemokine CCR8-I-309.
Authors: Alexis D Greene; Jessica A Kendziorski; Jeanette M Buckholz; Liang Niu; Changchun Xie; Susan M Pinney; Katherine A Burns Journal: Reprod Toxicol Date: 2018-12-21 Impact factor: 3.143