Volume 58, Issue 4 pp. 330-343

Gene Expression Profiling of the Rat Endometriosis Model

Ryo Konno

Ryo Konno

Department of Gynecology, Omiya Medical Center Jichi Medical University, Amanuma-cho, Omiya, Saitama, Japan;

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Hiroyuki Fujiwara

Hiroyuki Fujiwara

Department of Gynecology, Omiya Medical Center Jichi Medical University, Amanuma-cho, Omiya, Saitama, Japan;

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Sachiho Netsu

Sachiho Netsu

Department of Gynecology, Omiya Medical Center Jichi Medical University, Amanuma-cho, Omiya, Saitama, Japan;

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Kohei Odagiri

Kohei Odagiri

Department of Gynecology, Omiya Medical Center Jichi Medical University, Amanuma-cho, Omiya, Saitama, Japan;

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Miyuki Shimane

Miyuki Shimane

Laboratory of System Biology and Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan;

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Hitoshi Nomura

Hitoshi Nomura

Laboratory of System Biology and Medicine, Research Center for Advanced Science and Technology, The University of Tokyo, Tokyo, Japan;

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Mitsuaki Suzuki

Mitsuaki Suzuki

Department of Obstetrics and Gynecology, Jichi Medical University, Shimotuske, Tochigi, Japan

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First published: 06 August 2007
Citations: 44
Ryo Konno, MD, Department of Gynecology, Omiya Medical Center Jichi Medical University, Amanuma-cho, Omiya, Saitama 330-8503, Japan.
E-mail: [email protected]

Abstract

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.

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