Articles written in Journal of Biosciences

    • Estrogen is essential but not sufficient to induce endometriosis


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      Endometriosis is a common gynaecological disorder of unknown aetiology. Among the several factors, estrogen hasbeen implicated as a causative factor in endometriosis. In the present study using mouse model, we assessed the role ofestrogen in the initial implantation and growth of endometrium in ectopic locations. Uterine tissues from greenfluorescent protein (GFP) mice were transplanted in to the peritoneum of wild type mice in presence and absence ofestrogen. As compared to untreated controls, the implantation of uterine tissue at ectopic locations was higher whenestrogen was administered to both host and donor animals. However, this effect was not sustained as lesions regressedwithin 14 days of treatment. Irrespective of the treatment, peritoneal adipose was the most preferred site of lesionestablishment. The lesions did not have typical features of the endometriosis (presence of glands and stroma) even afterestrogen treatment and the ectopic tissue underwent regression by apoptosis irrespective of treatment. Since estrogenpromotes implantation of endometrial tissue to ectopic locations but failure of these ectopic lesions to grow and sustaineven in high estrogenic environment we propose that estrogen is necessary but not sufficient to sustain endometriosis.

    • Mouse model for endometriosis is characterized by proliferation and inflammation but not epithelial-to-mesenchymal transition and fibrosis


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      Endometriosis is a common disorder of unknown etiology, and non-surgical therapies are still a challenge. Tounderstand the pathogenesis and preclinical testing of drugs for endometriosis, animal models are highlydesirous. Herein, we carried out longitudinal characterization of a mouse model for endometriosis whereuterine tissue was transplanted onto the intestinal mesentery. During the course of lesion development from day15 to 60 post-induction, the ectopic endometrium became pale, fluid-filled and the animals developed peritonealadhesions. Most lesions resembled a well-differentiated type of endometriosis and ~13% of animalshad mixed type of lesions. There was extensive stromal compaction in the ectopic tissue. During the progressionof endometriosis, there was increased proliferation of epithelial and stromal cells as evident by PCNAstaining. Cyp19a1 (aromatase) mRNA was detected in the ectopic lesions on day 15 and 30 post-induction ofendometriosis, by day 60 the expression was reduced. As compared to the control endometrium, the mRNAlevels of Esr1 progressively reduced while the levels of inflammation associated genes (Esr2, Ifng, Tnf andIl1b) increased in the ectopic lesions. Infiltration of macrophages and polymorphonuclear leucocytes was alsoobserved in the ectopic lesions indicative of inflammation. As compared to control, there was no change inlevels of Cytokeratin and E-cadherin in the epithelial cells of ectopic endometrium. We did not observeexcessive collagen deposition or alpha-SMA positive myofibroblasts in the stroma of the ectopic endometrium.Thus, epithelial-to-mesenchymal transition and fibrosis are not detected in the mouse model of endometriosis.Our results show that the mouse model of endometriosis mimics some but not all the features of humanendometriosis.

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