Results
| PMID | 21111772 |
| Gene Name | TIMP4 |
| Condition | Endometriosis |
| Association |
Assocaited |
| Sex | Female |
| Associated genes | PGE2, COX-2, MMP1, MMP2, MMP3, MMP7, MMP9, TIMP1, TIMP2, TIMP3, TIMP4 |
| Other associated phenotypes |
Endometriosis |
|
Mol Cell Endocrinol. 2011 Jan 30;332(1-2):306-13. doi: 10.1016/j.mce.2010.11.022. Lee, JeHoon| Banu, Sakhila K| Subbarao, Thenmozhi| Starzinski-Powitz, Anna| Arosh, Joe A Reproductive Endocrinology and Cell Signaling Laboratory, Department of Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, TX 77843, United States. Prostaglandin E2 (PGE2) plays an important role in the pathogenesis of endometriosis. We recently reported that inhibition of COX-2 decreased migration as well as invasion of human endometriotic epithelial and stromal cells. Results of the present study indicates that selective inhibition of PGE2 receptors EP2 and EP4 suppresses expression and/or activity of MMP1, MMP2, MMP3, MMP7 and MMP9 proteins and increases expression of TIMP1, TIMP2, TIMP3, and TIMP4 proteins and thereby decreases migration and invasion of human immortalized endometriotic epithelial and stromal cells into matrigel. The interactions between EP2/EP4 and MMPs are mediated through Src and beta-arrestin 1 protein complex involving MT1-MMP and EMMPRIN in human endometriotic cells. These novel findings provide an important molecular and cellular framework for further evaluation of selective inhibition of EP2 and EP4 as potential nonsteroidal therapy for endometriosis in childbearing-age women. Mesh Terms: Cell Movement/physiology| Cells, Cultured| Dinoprostone/metabolism| Endometriosis/metabolism/pathology| Endometrium/*cytology| Epithelial Cells/metabolism/*pathology| Female| Humans| *Matrix Metalloproteinase Inhibitors| RNA, Small Interfering/me |
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