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Gene Expression Profiling of the Rat Endometriosis Model
Author(s) -
Konno Ryo,
Fujiwara Hiroyuki,
Netsu Sachiho,
Odagiri Kohei,
Shimane Miyuki,
Nomura Hitoshi,
Suzuki Mitsuaki
Publication year - 2007
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2007.00507.x
Subject(s) - endometriosis , osteopontin , pathogenesis , gene expression profiling , gene expression , gene , biology , immunohistochemistry , microarray , andrology , cancer research , pathology , peritoneal cavity , downregulation and upregulation , cell adhesion molecule , medicine , immunology , anatomy , biochemistry
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.