Matrix metalloproteinases (MMPs), especially the gelatinases MMP-2 and MMP-9, play a crucial role in the pathogenesis of endometriosis by enabling invasion.
Additionally, we performed two meta-analyses for MMP9rs3918242 polymorphism in endometriosis/adenomyosis and preeclampsia but found no association with either disorder.
MiR-33b can mediate cell apoptosis, alter VEGF and MMP-9 expression and affect proliferation and apoptosis of uterus endometrial cells, thus participating endometriosis formation.
G protein-coupled estrogen receptor stabilizes HIF-1α and thus promotes HIF-1α-induced VEGF and MMP9 in ESCs, which play critical roles in endometriosis.
Matrix metalloproteinase-2 (MMP-2), MMP-9, tissue inhibitor of matrix metalloproteinases (TIMP-1) and transforming growth factor-β2 (TGF-β2) expression in eutopic endometrium of women with peritoneal endometriosis.
Treatment with PKF 115-584 inhibited MMP-9 activity to undetectable levels in both menstrual endometrial epithelial and stromal cells of patients with endometriosis.
Immunohistochemical staining with the streptavidin-peroxidase method was conducted to determine the expression of GPR30 and MMP-9 in 24 cases of endometriosis-associated ovarian carcinoma (EAOC) and 32 specimens of ovarian endometriosis without malignant transformation.
We used quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) to quantify the mRNA levels of vascular endothelial growth factor A (VEGFA), matrix metalloproteinase-3 (MMP-3), and MMP-9 in peripheral blood from 20 patients with mild/intermediate endometriosis, 20 patients with severe endometriosis and 20 endometriosis-free subjects.
The results demonstrated that polymorphisms in MMP-2 (-735 C/T) and MMP-9 (-1562 C/T) were associated with elevated risk of endometriosis and that certain MMP-2 promoter haplotypes were more common in control group.
Both endometrial stromal cells (ESCs) and the combination of 17beta-estradiol and TCDD increase the secretion of TECK in the endometriosis-associated cells and promote the invasiveness of ESCs by increasing expression of matrix metalloproteinase (MMP)-2 and MMP-9.
Higher expression of vascular endothelial growth factor (VEGF) and its receptor VEGFR-2 (Flk-1) and metalloproteinase-9 (MMP-9) in a rat model of peritoneal endometriosis is similar to cancer diseases.
Frequencies of genotypes and haplotypes were compared with the risk of endometriosis including -1562C>T, R279Q, P574R, and R668Q polymorphisms of MMP-9.
The combination of TNF and MMP9 increased the sICAM1 concentration 14-fold in the endometriosis cell media, whereas GM6001 inhibited the stimulatory effect of TNF in both cell cultures.
c-fos protein was predominantly located in the nuclei of glandular epithelial cells and stromal cells. c-fos and MMP-9 protein levels in paired eutopic and ectopic endometria from women with endometriosis were significantly higher than those in the endometrium from women without endometriosis.
MMP-2 and MMP-9, and E-cadherin expressions were significantly higher and beta-catenin expression was significantly lower in endometriosis as compared to endometrioid carcinoma.
We conclude that MMP-7-181A/G polymorphism has a potential to be a susceptibility factor for endometriosis and adenomyosis while MMP-9-1562C/T polymorphism may not provide a useful marker to predict susceptibility to endometriosis and adenomyosis, at least in women from North China.
These findings make plausible the involvement of MMP-9/TIMP-1 imbalance in the invasiveness of the endometrial tissue of patients with endometriosis and the ectopic development of the disease.