Induction of endometriosis in marmoset monkeys

In: Experimental and Clinical Endocrinology & Diabetes · 2005 · vol. 113(S 1) · doi:10.1055/s-2005-862824 · W2624137174
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This study established an endometriosis model in female marmoset monkeys by injecting endometrium, confirming the development of vascularized endometriotic foci containing endometrial glandular tissue and stroma.

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This study investigated the artificial induction of endometriosis in female marmoset monkeys to establish a relevant primate model for human disease. Researchers injected autologous endometrium into the intrapelvic cavity and monitored the animals over two years using endocrine parameters, color Doppler ultrasonography, and histological analysis. The results demonstrated that endometriotic foci developed primarily on the bladder, ovaries, and uterus, exhibiting increased vascular supply and confirming tissue origin through steroid receptor expression and molecular markers. This paper is centrally about endometriosis — specifically the successful experimental induction of the condition in a non-human primate model.

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Abstract

Endometriosis is not only a chronic painful disease, but also one of the most common causes of infertility. However, current therapeutic approaches are insufficient and etiology of endometriosis is uncertain. Most critical to gain more knowledge about this disease is an appropriate animal model. In this study, female marmoset monkeys (n=10), aged more than 6 years, were exposed to different experimental procedures for intrapelvic injection of endometrium by uterine flushing at several time points throughout an experimental period of 2 years. Ovarian cycle length was monitored by endocrine parameters and blood flow of the reproductive organs was analysed by colour Doppler ultrasonography. First "endometriotic foci" were detected by ultrasound after 5 months treatment. They were then surgically removed and analysed by histology, immunohistochemistry and molecular biology. Clinical symptoms observed in treated monkeys were irregular cycles and occurence of ovarian cysts. Colour doppler examination showed increase of vascular supply in "endometriotic foci", which were mainly located at the bladder, the ovaries und the uterus. The presence of glandular tissue and stromal fibroblasts of endometrial origin was confirmed by histology as well as by expression patterns of steroid receptors, steroidogenic enzymes and VEGF.
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Subscribe to RSS DOI: 10.1055/s-2005-862824 Induction of endometriosis in marmoset monkeys Endometriosis is not only a chronic painful disease, but also one of the most common causes of infertility. However, current therapeutic approaches are insufficient and etiology of endometriosis is uncertain. Most critical to gain more knowledge about this disease is an appropriate animal model. In this study, female marmoset monkeys (n=10), aged more than 6 years, were exposed to different experimental procedures for intrapelvic injection of endometrium by uterine flushing at several time points throughout an experimental period of 2 years. Ovarian cycle length was monitored by endocrine parameters and blood flow of the reproductive organs was analysed by colour Doppler ultrasonography. First “endometriotic foci“ were detected by ultrasound after 5 months treatment. They were then surgically removed and analysed by histology, immunohistochemistry and molecular biology. Clinical symptoms observed in treated monkeys were irregular cycles and occurence of ovarian cysts. Colour doppler examination showed increase of vascular supply in “endometriotic foci“, which were mainly located at the bladder, the ovaries und the uterus. The presence of glandular tissue and stromal fibroblasts of endometrial origin was confirmed by histology as well as by expression patterns of steroid receptors, steroidogenic enzymes and VEGF. In summary, our data suggest that endometriosis can artificially be induced in the marmoset monkey at preferential peritoneal locations. Thus, the marmoset provides a useful and unique primate model for the human disease. This project was supported by SOLVAY Pharmaceuticals GmbH.

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