Aberrant gene expression profile in a mouse model of endometriosis mirrors that observed in women

被引:48
作者
Pelch, Katherine E. [1 ]
Schroder, Amy L. [1 ]
Kimball, Paul A. [1 ]
Sharpe-Timms, Kathy L. [1 ]
Davis, J. Wade [2 ,3 ]
Nagel, Susan C. [1 ]
机构
[1] Univ Missouri, Dept Obstet Gynecol & Womens Hlth, Columbia, MO 65212 USA
[2] Univ Missouri, Dept Hlth Management & Informat, Columbia, MO 65212 USA
[3] Univ Missouri, Dept Stat, Columbia, MO 65212 USA
基金
美国国家卫生研究院;
关键词
Endometriosis; mouse model; gene expression profile; MATRIX-METALLOPROTEINASE EXPRESSION; STEROID-RECEPTOR EXPRESSION; DIFFERENTIAL EXPRESSION; PROLIFERATIVE ACTIVITY; MICROARRAY ANALYSIS; STROMAL CELLS; PERITONEAL; HAPTOGLOBIN; IMPLANTS; ESTROGEN;
D O I
10.1016/j.fertnstert.2009.03.086
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective: To define the altered gene expression profile of endometriotic lesions in a mouse model of surgically induced endometriosis. Design: Autologous experimental mouse model. Setting: Medical school department. Animal(s): Adult C57B16 mice. Intervention(s): Endometriosis was surgically induced by autotransplantation of uterine tissue to the intestinal mesentery. Endometriotic lesions and eutopic uteri were recovered at 3 or 29 days after induction. Main Outcome Measure(s): Altered gene expression was measured in the endometriotic lesion relative to the eutopic uterus by genome-wide complementary DNA microarray analysis and was confirmed by real-time reverse transcriptase polymerase chain reaction for six genes. Relevant categories of altered genes were identified using gene ontology analysis to determine groups of genes enriched for altered expression. Result(s): The expression of 479 and 114 genes was altered in the endometriotic lesion compared with the eutopic uterus at 3 or 29 days after induction, respectively. Gene ontology enrichment analysis revealed that genes associated with the extracellular matrix, cell adhesions, immune function, cell growth, and angiogenesis were altered in the endometriotic lesion compared with the eutopic uterus. Conclusion(s): According to gene expression analysis, the mouse model of surgically induced endometriosis is a good model for studying the pathophysiology and treatment of endometriosis. (Fertil Steril (R) 2010;93:1615-27. (C)2010 by American Society for Reproductive Medicine.)
引用
收藏
页码:1615 / 1627
页数:13
相关论文
共 64 条
[21]   Genetic or enzymatic disruption of aromatase inhibits the growth of ectopic uterine tissue [J].
Fang, ZJ ;
Yang, SJ ;
Gurates, B ;
Tamura, M ;
Simpson, E ;
Evans, D ;
Bulun, SE .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 2002, 87 (07) :3460-3466
[22]   A modified baboon model for endometriosis [J].
Fazleabas, AT ;
Brudney, A ;
Gurates, B ;
Chai, D ;
Bulun, S .
ENDOMETRIOSIS: EMERGING RESEARCH AND INTERVENTION STRATEGIES, 2002, 955 :308-317
[23]  
Fernandes T, 2008, EUR J GYNAECOL ONCOL, V29, P341
[24]   Molecular profiling of experimental endometriosis identified gene expression patterns in common with human disease [J].
Flores, Idhaliz ;
Rivera, Elizabeth ;
Ruiz, Lynnette A. ;
Santiago, Olga I. ;
Vernon, Michael W. ;
Appleyard, Caroline B. .
FERTILITY AND STERILITY, 2007, 87 (05) :1180-1199
[25]   Peritoneal environment, cytokines and angiogenesis in the pathophysiology of endometriosis [J].
Gazvani, R ;
Templeton, A .
REPRODUCTION, 2002, 123 (02) :217-226
[26]   Endometriosis [J].
Giudice, LC ;
Kao, LC .
LANCET, 2004, 364 (9447) :1789-1799
[27]   The rodent estrous cycle: Characterization of vaginal cytology and its utility in toxicological studies [J].
Goldman, Jerome M. ;
Murr, Ashley S. ;
Cooper, Ralph L. .
BIRTH DEFECTS RESEARCH PART B-DEVELOPMENTAL AND REPRODUCTIVE TOXICOLOGY, 2007, 80 (02) :84-97
[28]  
Grümmer R, 2006, HUM REPROD UPDATE, V12, P641, DOI 10.1093/humupd/dml026
[29]  
HALME J, 1984, OBSTET GYNECOL, V64, P151
[30]   Apoptosis and endometriosis [J].
Harada, Tasuku ;
Taniguchi, Fuminori ;
Izawa, Masao ;
Ohama, Yoko ;
Takenaka, Yasuko ;
Tagashira, Yukiko ;
Ikeda, Ayako ;
Watanabe, Ayako ;
Iwabe, Tomio ;
Terakawa, Naoki .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2007, 12 :3140-3151