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Reviews: in vitro models to study the pathogenesis of endometriosis. | LitMetric

Reviews: in vitro models to study the pathogenesis of endometriosis.

Reprod Sci

Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology and Infertility, University of Texas Health Science Center San Antonio, San Antonio, Texas 78229, USA.

Published: January 2010

AI Article Synopsis

  • Several in vitro models have been created to mimic the intraperitoneal environment for studying endometriosis, including the use of chicken chorioallantoic membrane and human tissue models such as amniotic membrane and peritoneal explants.
  • These models allow researchers to examine how endometrial cells attach to and invade peritoneal mesothelial cells, and assess the influence of cytokines on early lesion development.
  • Two- and three-dimensional invasion chamber models are highlighted as tools to study cell interactions and explore potential new treatments for endometriosis.

Article Abstract

Several in vitro models that attempt to replicate the intraperitoneal environment have been developed to study the pathogenesis of endometriosis. The chicken chorioallantotic membrane has been used, but it has not been well characterized and may introduce some species specific variables. In vitro models using human tissues include amniotic membrane, human peritoneal explants, and cell culture monolayers. These models have been used to qualitatively, quantitatively, and temporally assess attachment of endometrial cells to peritoneal mesothelial and subsequent transmesothelial invasion. These models have also been used to assess the role of cytokines in the development of the early endometriotic lesion. Two- and three dimensional invasion chamber models have been utilized to assess endometrial cell interactions with peritoneal mesothelial cells and the extracellular matrix. Invasion models are also useful to evaluate novel therapeutic approaches. This review will focus on the above models to assist reproductive scientists interested in the pathogenesis of endometriosis.

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Source
http://dx.doi.org/10.1177/1933719109338221DOI Listing

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