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  • Title: Ectopic, autologous eutopic and normal endometrial stromal cells have altered expression and chemotactic activity of RANTES.
    Author: Fang CL, Han SP, Fu SL, Wang W, Kong N, Wang XL.
    Journal: Eur J Obstet Gynecol Reprod Biol; 2009 Mar; 143(1):55-60. PubMed ID: 19157676.
    Abstract:
    OBJECTIVE: To evaluate if the expression and chemotactic activity of RANTES are different in IL-1beta treated autologous eutopic endometrial stromal cells compared to ectopic and normal endometrium. STUDY DESIGN: Conditioned media from IL-1beta-treated ectopic, autologous eutopic and normal endometrial stromal cells were analyzed with a specific sandwich ELISA to quantify RANTES. The monocyte chemotactic activity of RANTES was assayed in a Boyden Chamber. RESULTS: RANTES expression in IL-1beta-treated autologous eutopic and normal endometrial stromal cells was significantly lower than ectopic endometrium. Autologous eutopic endometrial stromal cells showed a significant increase in RANTES expression compared to normal endometrium after IL-1beta stimulation for 60 h. The monocyte chemotactic activities of these conditioned media were highly correlated with the immunoreactive RANTES concentration. We observed significantly increased monocyte chemotactic activity in conditioned media of ectopic stromal cells compared to autologous eutopic and normal endometrium. The different chemotactic activity of RANTES between the autologous eutopic and normal endometrial stromal cells was also statistically significant. RANTES accounts for the majority (62%) of the monocyte chemotactic activity in ectopic endometrial stromal cells conditioned media and 55% of that activity in autologous eutopic endometrium. CONCLUSIONS: Although the eutopic endometric of women with and without endometriosis are histologically similar, our findings confirm that different expression and chemotactic activity of RANTES exist between autologous eutopic and normal endometrium. The altered expression of RANTES and monocyte chemotactic activity observed in ectopic, autologous eutopic and normal endometrium suggest the autologous eutopic endometrium may contribute to the pathogenesis of endometriosis.
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