OBJECTIVE: Endometriosis is characterized by the ectopic growth of endometrial tissue. One of the first steps to the spread of endometriosis in the peritoneal cavity is the attachment of endometriotic cells to peritoneal surfaces after they have been released into the peritoneal fluid from pre-existing endometriotic lesions. The increased adhesive and proliferative potential of endometriotic cells in response to specific extracellular matrix (ECM) components has been suggested to contribute to the pathogenesis of endometriosis. STUDY DESIGN: Adhesive properties of endometriotic stromal cells (ECSC) and normal eutopic endometrial cells (NESC) to various extracellular matrix proteins were investigated by in vitro cell adhesion assays. The expression levels of integrins in these cells were also examined by Western blot analysis. RESULTS: Both ECSC and NESC significantly adhered to collagen type I and collagen type IV. ECSC revealed higher adhesive properties to these ECM proteins than NESC did. ECSC, but not NESC, adhered to fibronectin and laminin. Higher levels integrin of α1, α2, αv, β1, and β3 protein expression were observed in ECSC than in NESC. On the other hand, the levels of integrin α3 and αL proteins were lower in ECSC than in NESC. CONCLUSIONS: The results suggest that endometriotic cells possess stronger adhesion to ECM proteins, and that increase may be mediated, in part, through integrins. These findings may elucidate one of the mechanisms underlying the formation of peritoneal endometriotic lesions.
OBJECTIVE:Endometriosis is characterized by the ectopic growth of endometrial tissue. One of the first steps to the spread of endometriosis in the peritoneal cavity is the attachment of endometriotic cells to peritoneal surfaces after they have been released into the peritoneal fluid from pre-existing endometriotic lesions. The increased adhesive and proliferative potential of endometriotic cells in response to specific extracellular matrix (ECM) components has been suggested to contribute to the pathogenesis of endometriosis. STUDY DESIGN: Adhesive properties of endometriotic stromal cells (ECSC) and normal eutopic endometrial cells (NESC) to various extracellular matrix proteins were investigated by in vitro cell adhesion assays. The expression levels of integrins in these cells were also examined by Western blot analysis. RESULTS: Both ECSC and NESC significantly adhered to collagen type I and collagen type IV. ECSC revealed higher adhesive properties to these ECM proteins than NESC did. ECSC, but not NESC, adhered to fibronectin and laminin. Higher levels integrin of α1, α2, αv, β1, and β3 protein expression were observed in ECSC than in NESC. On the other hand, the levels of integrin α3 and αL proteins were lower in ECSC than in NESC. CONCLUSIONS: The results suggest that endometriotic cells possess stronger adhesion to ECM proteins, and that increase may be mediated, in part, through integrins. These findings may elucidate one of the mechanisms underlying the formation of peritoneal endometriotic lesions.
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