Use this URL to cite or link to this record in EThOS: http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.604767
Title: An in vivo model of endometriosis
Author: Hull, M. L.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 2006
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Abstract:
The nude mouse model of endometriosis was used to study the longitudinal integration of human endometrium at an ectopic site. Histological, morphometric and immunohistochemical techniques were used to investigate nude mouse lesion development. Seven days after endometrial implantation, central necrosis and glandular degeneration were invariably seen in nude mouse lesions. By day 14, tissue remodelling had occurred and a novel vasculature was apparent. Affymetrix microarray GeneChips were used to ascertain the peritoneal transcriptome of nude mouse lesions. mRNA sequences not previously associated with endometriotic lesion development were detected, including some linked to osteoblast activity. techniques to verify the murine origin of these transcripts were developed. A selective cyclooxygenase-2 (COX-2) inhibitor and anti-angiogenic agents were tested in the nude mouse model of endometriosis. COX-2 can modulate inflammation, angiogenesis and cellular proliferation, which were observed in developing nude mouse lesions. However, the quantity and volume of lesions remained unaltered in mice treated with a COX-2 inhibitor. In contrast, when agents that inhibited vascular endothelial growth factor were administered to nude mice, the number of lesions was reduced. This thesis provides the first comprehensive description of the cellular and molecular events that occur during endometriosis-like lesion development. Disruption of only one aspect of this process (neovascularisation) revealed the therapeutic potential of anti-angiogenic agents in endometriotic disease. Many other transcripts and cells were identified that may be critical to nude mouse lesion establishment. Future research directed towards functional suppression of these factors may inhibit endometriotic lesions and increase treatment options for women with endometriosis.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID: uk.bl.ethos.604767  DOI: Not available
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