Gene expression profiling of the rat endometriosis model.

Problem: To investigate the molecular mechanism of endometriosis, gene expression profiling was analyzed in a rat endometriosis model.
Method of Study: An endometriosis model was induced by uterine autotransplantation in the peritoneal cavity on a female-SD rat (8 weeks old). As control samples, the normal uterine tissues were used. The gene expression was compared between endometriotic lesions and normal uterine tissues by cDNA microarray analysis, quantitative real time RT-PCR and immunohistochemistry.
Results: The expression of 71 genes was upregulated and that of 45 genes was downregulated in the endometriotic lesions compared to normal uterine tissues. The upregulated genes included genes encoding cytokines, chemokines, growth factors and cell adhesion molecules. The levels of transcripts of osteopontin, Lyn, Vav1, Runx1, and l-selectin in the endometriotic lesions were 130, 10, 10, 12 and 46-fold higher than the respective levels in the eutopic endometrial samples.
Conclusion: The results suggest that osteopontin, Lyn, Vav1, Runx1, and l-selectin play important roles in the pathogenesis of endometriosis.