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Pathogenesis of endometriosis--current research
Craig A Witz1, Karen T Allsup, Iris A Montoya-Rodriguez
1Department of Obstetrics and Gynecology, The University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA.
Human Fertility (Cambridge, England)
|March 29, 2003
Summary
Endometrial cells rapidly adhere to and invade the mesothelium, suggesting surface molecules are key in endometriosis development. Hyaluronidase inhibition points to CD44-hyaluronan binding as a significant factor in early lesion formation.
Area of Science:
- Gynecology
- Cell Biology
- Pathogenesis Research
Background:
- Endometriosis involves endometrial tissue outside the uterus, often on peritoneal surfaces.
- The interaction between endometrial cells and the peritoneum is crucial for lesion establishment.
Purpose of the Study:
- To investigate the adherence and invasion of endometrial cells to peritoneal mesothelium.
- To identify molecular mechanisms involved in the early pathogenesis of endometriosis.
Main Methods:
- Co-culture of endometrial cells (stroma and epithelium) with mesothelial cells and monolayers.
- Time-course analysis of endometrial cell attachment and transmesothelial invasion.
- Assessment of hyaluronidase inhibition on endometrial cell adherence.
Main Results:
- Endometrial cells readily adhere to intact mesothelium and mesothelial monolayers.
- Attachment occurs rapidly (within 1 hour), with invasion between 1-24 hours.
- Hyaluronidase significantly inhibits endometrial cell adherence, implicating CD44-hyaluronan interactions.
Conclusions:
- The mesothelium is not a non-adherent surface for endometrial cells.
- Surface molecules on mesothelial cells play a role in early endometriotic lesion formation.
- CD44-hyaluronan binding is a key mechanism in endometriosis pathogenesis, warranting further investigation of mesothelial adhesion molecules.