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Reproductive Molecular Research Group,5 Department of Pathology, University of Cambridge, Cambridge CB2 1QP, United Kingdom
Department of Obstetrics and Gynaecology,6 University of Cambridge Clinical School, The Rosie Hospital, Cambridge CB2 2SW, United Kingdom
ABSTRACT
The endometrium is a dynamic tissue that undergoes periodic growth, remodeling and breakdown under the influence of ovarian steroid hormones. To investigate the molecular mechanisms underlying these processes, we used a murine model to mimic the decidualization and regression observed in humans. Ovariectomized mice were treated sequentially with steroid hormones, and subsequently, to induce decidualization, oil was injected into the uterine lumen. The animals were then divided into progesterone-maintained and progesterone-withdrawal groups. In the latter group, a process similar to menstruation was induced. The uterine tissues were collected at several time-points after the induction of decidualization. Histological analysis demonstrated that decidualization and tissue degeneration were successfully induced with similar features to those observed during the human menstrual cycle. Immunohistochemical, morphometric, and microarray-based techniques were used to study the cellular and molecular changes. The volume fractions of leukocytes, macrophages, and neutrophils, but not endothelial cells, increased in decidualized uteri and decreased after major tissue degradation was completed. The microarray data show that the levels of many transcripts that encode immune-related factors changed during the time-course used for this model, and the transcript levels of many of these factors paralleled the changes observed in the volume fractions of the immune cells. The results of the present study suggest that this model is a useful alternative to the use of non-human primates. Our findings also show that immune cells are recruited into the menstruating endometrium, and that immune-related genes are regulated in the uterus throughout menstruation.
female reproductive tract, growth hormone, immunology, uterus
3Current address: Faculty of Medicine, Level 2, Faculty Building, South Kensington Campus, Imperial College. London, SW7 2AZ, United Kingdom.
4Current address: Department of Molecular Medicine & Pathology, School of Medical Sciences, University of Auckland, Private Bag 92019, Auckland, New Zealand.
1Supported by the UK Medical Research Council (MRC) Programme grant G9623012 to D.S.C.J., S.K.S., and C.G.P. The cDNA microarray data have been deposited in the EBI ArrayExpress Database (http://www.ebi.ac.uk/arrayexpress/) and are accessible through accession number E-MEXP-932. The Affymetrix microarray data have been deposited in the NCBI Gene Expression Omnibus (http://www.ncbi.nlm.nih.gov/geo/) and are accessible through GEO Series accession number GSE6359.
Correspondence: 2Ching-wen Cheng, Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge, CB2 1QP, United Kingdom FAX: 44 1223 333346; e-mail: cwc28{at}cam.ac.uk
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  M. L. Hull, C. R. Escareno, J. M. Godsland, J. R. Doig, C. M. Johnson, S. C. Phillips, S. K. Smith, S. Tavare, C. G. Print, and D. S. Charnock-Jones Endometrial-Peritoneal Interactions during Endometriotic Lesion Establishment Am. J. Pathol., September 1, 2008; 173(3): 700 - 715. [Abstract] [Full Text] [PDF]
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