An in vivo-model to investigate therapeutical approaches for the treatment of peritoneal endometriosis

S Fechner, F Schwarzer, Isabella Gashaw, M Schmidt, Elke Winterhager, Ruth Grümmer
In: Experimental and Clinical Endocrinology & Diabetes · 2005 · vol. 113(S 1) · doi:10.1055/s-2005-862819 · W2621980318
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⚙ AI-generated summary by claude@2026-06, 2026-06-12 ⓘ

Researchers transplanted human endometrial tissue into nude mice, finding it persisted for 28 days with vascularization and hormone receptor expression, and demonstrated that gestagen, antigestagen, and danazol regulated these in the lesions.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-12 · read from full text ⓘ

The study aimed to establish and use an in vivo mouse model to examine mechanisms sustaining peritoneal endometriotic lesions, focusing on angiogenesis and estrogen-related pathways. Human endometrial tissue was transplanted into the peritoneal cavity of nude mice, and after implantation (2–28 days) investigators assessed neoangiogenesis and the expression of steroid hormone receptors and estrogen-converting enzymes, finding mouse vessel ingrowth beginning around day 4 that correlated with increased VEGF/bFGF transcripts and receptors. The lesions maintained morphology and expressed differentiation markers, estrogen receptor alpha, progesterone receptors, and various estrogen-converting enzymes. The authors explicitly frame this as an experimental model for evaluating cell biological mechanisms and therapeutic approaches, without claiming it reproduces all aspects of human endometriosis. This paper is centrally about endometriosis — it develops and applies an in vivo-model using peritoneal transplantation of human endometrial tissue to study angiogenesis and hormone regulation in endometriotic lesions.

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Abstract

Endometriosis is a common gynecologic disorder characterized by the presence of endometrial tissue outside the uterus. The disease is associated with dysmenorrhea, pelvic pain and infertility, but the cell biological mechanisms involved in the pathogenesis are yet not understood. It is known that angiogenesis is a prerequisite for the maintenance of endometriotic lesions and it is discussed that an elevated estrogen concentration within the ectopic lesions may support their persistance. To investigate the role of those parameters for the maintenance of ectopic endometrial lesions, we established an in-vivo-model by transplanting human endometrial tissue into the peritoneal cavity of nude mice. At 2 to 28 days after implantation angiogenesis as well as the expression of steroid hormone receptors and estrogen-converting enzymes were investigated in the endometriotic lesions. Neoangiogenesis of mouse vessels into the human endometrial fragments occurred from day 4 after transplantation onwards. This correlated to an increase in transcripts of VEGF and bFGF as well as of their specific receptors. The lesions revealed a well preserved morphology up to 28 days, expression of differentiation markers, of estrogen receptor alpha, progesterone receptors and of different estrogen converting enzymes. We demonstrated that in this in vivo model the expression of steroid hormone receptors as well as of aromatase was regulated in the human ectopic endometrial lesions by systemic application of gestagen, antigestagen (RU486) and the gonadotropin inhibitor danazol. Thus we could show that culturing of human endometrial tissues in the peritoneal cavity of nude mice is an useful experimental model to evaluate cell biological mechanisms responsible for the persistence of ectopic endometrium in the peritoneal cavity.
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Subscribe to RSS DOI: 10.1055/s-2005-862819 An in vivo-model to investigate therapeutical approaches for the treatment of peritoneal endometriosis Endometriosis is a common gynecologic disorder characterized by the presence of endometrial tissue outside the uterus. The disease is associated with dysmenorrhea, pelvic pain and infertility, but the cell biological mechanisms involved in the pathogenesis are yet not understood. It is known that angiogenesis is a prerequisite for the maintenance of endometriotic lesions and it is discussed that an elevated estrogen concentration within the ectopic lesions may support their persistance. To investigate the role of those parameters for the maintenance of ectopic endometrial lesions, we established an in-vivo-model by transplanting human endometrial tissue into the peritoneal cavity of nude mice. At 2 to 28 days after implantation angiogenesis as well as the expression of steroid hormone receptors and estrogen-converting enzymes were investigated in the endometriotic lesions. Neoangiogenesis of mouse vessels into the human endometrial fragments occurred from day 4 after transplantation onwards. This correlated to an increase in transcripts of VEGF and bFGF as well as of their specific receptors. The lesions revealed a well preserved morphology up to 28 days, expression of differentiation markers, of estrogen receptor alpha, progesterone receptors and of different estrogen converting enzymes. We demonstrated that in this in vivo model the expression of steroid hormone receptors as well as of aromatase was regulated in the human ectopic endometrial lesions by systemic application of gestagen, antigestagen (RU486) and the gonadotropin inhibitor danazol. Thus we could show that culturing of human endometrial tissues in the peritoneal cavity of nude mice is an useful experimental model to evaluate cell biological mechanisms responsible for the persistence of ectopic endometrium in the peritoneal cavity.

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endometriosisdysmenorrheainfertility

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