Endometriosis Knowledgebase


A repository for genes associated with endometriosis

Results


PMID 26656198
Gene Name MMP9
Condition Endometriosis
Association Associated
Population size 6
Population details 6 endometriosis patients
Sex Female
Associated genes MMP9, TIMP1, VEGFA
Other associated phenotypes Endometriosis
Overexpression of a steroid receptor-binding protein bearing the regulator of the G-protein signaling domain suppresses migration and invasion of human endometrial stromal cells stimulated by 17beta-estradiol.

Eur J Obstet Gynecol Reprod Biol. 2016 Jan;196:26-30. doi:

Xiong, Yu-fang| Xiong, Zhou-fang

Department of Biochemistry and Molecular Biology, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, PR China.| Department of Obstetrics and Gynecology, Union Hospital of Tongji Medical College, Huazhong University of

OBJECTIVE: Endometriosis is an estrogen-dependent disease, a steroid receptor-binding protein bearing the regulator of the G-protein signaling domain (SRB-RGS) can suppress the estrogen receptors-mediated transcriptional activities. We sought to determine whether overexpression of SRB-RGS suppresses the migration and invasion ability of endometrial stromal cells stimulated by 17beta-estradiol (E2). STUDY DESIGN: Endometrial stromal cells were obtained from endometriosis patients. SRB-RGS was overexpressed in the cells stimulated by E2. The migration and invasion ability of the cells were measured by migration assay and invasion assay, respectively. Western blot analysis was done to test the expression of matrix metalloproteinase-9 (MMP-9), tissue inhibitors of metalloproteinase-1 (TIMP-1) and vascular endothelial growth factor (VEGF). RESULTS: Overexpression of SRB-RGS suppressed the migration and invasion ability of the stromal cells stimulated by E2; it also suppressed the expression of MMP-9 and VEGF, while the expression of TIMP-1 was increased. CONCLUSIONS: Overexpression of SRB-RGS suppresses the migration and invasion ability of the E2-stimulated endometrial stromal cells. The molecular mechanism is the reduced expression of MMP-9 and VEGF, and the increased expression of TIMP-1. These findings suggest that the coding gene of SRB-RGS is a promising target gene for endometriosis gene therapy.

Mesh Terms: Adult| Cell Movement/drug effects/*physiology| Endometriosis/*metabolism/pathology| Estradiol/*pharmacology| Female| Humans| Matrix Metalloproteinase 9/metabolism| Stromal Cells/drug effects/*metabolism/pathology| Tissue Inhibitor of Metalloprotei