COX-2 over-expression may be a result of the malignant transformation of endometriosis to endometrioid type ovarian cancer or may represent an interaction between the two cellular components.
Cyclooxygenase-2 and VEGF were closely correlated with each other, and both of them appear to play a role in the angiogenesis of ovarian endometriosis.
COX-2 mRNA level in unmethylated endometrium of the endometriosis group or the control group was 2.39-fold and 2.66-fold, respectively, higher than that in the methylated endometrium of the same group (P < 0.01).
Also, COX-2 gene expression and prostaglandin E(2) production were induced in those cells by increasing COX-2 promoter transcription activity, which could be attenuated by a specific p38MAPK inhibitor, suggesting a role for peritoneal fluid in the etiopathogenesis of endometriosis.
Because DNG inhibits aromatase and COX-2 expression as well as PGE(2) production in ESCs, these pharmacologic features might contribute to a therapeutic effect of DNG on endometriosis.
Because overexpression of COX-2 has been demonstrated to be a master regulator in endometriosis progression, our data demonstrate the critical function of proinflammatory cytokines and the COUP-TFII regulatory gene network in the progression of endometriosis.
Btk inhibitor Ibrutinib prevented lesion growth, reduced mRNA expression of cyclooxygenase-2, alpha smooth muscle actin and type I collagen in the lesions and skewed activated B cells toward Bregs in the spleen and peritoneal cavity of mice with endometriosis.
By contrast, the cyclic stretch mimicking physiological peristalsis (3% elongation at 2 cycles/min) did not induce significant COX-2, mPGES-1 or PGE(2) production within 12 h. Both COX-2 and mPEGS-1 are PGE(2) synthases, and the aberrant COX-2 and PGE(2) production play important roles in the pathogenesis of endometriosis.
Case-control study to investigate the association between endometriosis and four inflammation-related genes: interleukin (IL)-6, IL-10, IL-1 beta, and cyclooxygenase-2.
Elevated Cox-2 expression in stromal cells in eutopic endometrium from patients with deep endometriosis may play a role in severe, endometriosis-related dysmenorrhea.
Expressions of COX-2 mRNA in endometrium, ectopic endometriosis tissue, and peritoneum were quantitavely determined by competitive reverse transcription-polymerase chain reaction (RT-PCR).
For the first time, decreased expression of PTGS2 was found in cumulus cells of infertile women with endometriosis compared with controls (7.2 ± 10.5 versus 12.4 ± 15.7), which might be related to reduced levels of COX-2 in the cumulus cells of women with the disease.
Herein, we report that macrophage migration inhibitory factor (MIF), a potent proinflammatory and growth-promoting factor found at elevated concentrations in the peritoneal fluid of women with endometriosis and active endometriosis lesions, acts directly on ectopic endometrial cells to stimulate the synthesis of COX-2, the inducible form of COX, and the release of PGE(2).
In a preclinical mouse model of endometriosis we demonstrated overexpression of the PGE<sub>2</sub>-signaling pathway (including COX-2, EP<sub>2</sub>, EP<sub>4</sub>) in endometriosis lesions, dorsal root ganglia (DRG), spinal cord, thalamus and forebrain.
In conclusion, our study establishes the involvement of MMP-2 activity via COX-2-PGE2-pAKT axis in promoting angiogenesis during endometriosis progression.
In patients with severe endometriosis who underwent fertility-sparing complete ablation, COX-2 overexpression characterizes a subgroup of patients with lower risk of relapse and longer relapse-free survival.
In the endometriotic lesions, prostaglandin E2 (PGE2) produced by cyclooxygenase-2 (COX-2), binds to its EP4 receptor (EP4), and via c-Src kinase induces MMPs activation, promoting endometriosis.