DNA microarray analysis in a mouse model for endometriosis and validation of candidate factors with human adenomyosis

详细信息    查看全文

• 作者：Ken Takeshi Kusakabe ; Hideaki Abe ; Tomohiro Kondo ; Keiko Kato ; Toshiya Okada ; Yoshinori Otsuki
• 关键词：Calbindin-D28k (CALB1) ; Cxcl10 (IP10) ; EP3 ; Endometriosis ; Prostaglandin I2 synthase
• 刊名：Journal of Reproductive Immunology
• 出版年：2010
• 出版时间：June 2010
• 年：2010
• 卷：85
• 期：2
• 页码：149-160
• 全文大小：1331 K

文摘

Gene expression profiling can be of benefit in identifying critical factors in the process of disease initiation and development. However, in endometriosis it has proven difficult to identify common genes between DNA microarray studies, presumably because of tissue homogeneity in lesions and diversity in the patients’ conditions. We attempted DNA microarray analysis in a mouse model for endometriosis with stable lesions and a homogeneous genetic background. Data extracted from the mouse model was then evaluated in human tissues. Mice of the ddY strain underwent surgery to remove the left side of the uterine horn, and the uterine tissue was then minced into small segments and auto-transplanted onto the left peritoneum. After 8 weeks, most of the uterine grafts were enlarged and had regenerated lumens. Comparison of the intensity of mRNA expression between grafts and normal uteri showed that genes encoding immune regulators (e.g. CXCL10) and metabolic factors (e.g. calbindin D-28K) were highly up-regulated in the grafts. Strongly inhibited genes in the grafts included prostaglandin-related factors [e.g. prostaglandin E receptor 3 (subtype EP3) and prostaglandin I2 synthase]. Variation in some candidate factors detected in the mouse model was observed by immunohistochemical studies in human adenomyosis tissues. The gene list in the present study is available for re-evaluation of past studies and provides new candidate factors potentially involved in the pathogenesis of endometriosis.