Influence of peritoneal fluid on the expression of angiogenic and proteolytic factors in cultures of endometrial cells from women with endometriosis.
BACKGROUND
Endometriosis, defined as the presence of endometrium outside the uterus, is one of the most frequent benign gynaecological diseases. It has been suggested that both endometrial and peritoneal factors, related to angiogenesis and proteolysis, can be implicated in this disease. The aim of this study was to evaluate the influence of peritoneal fluid on the expression of angiogenic and proteolytic factors in cultures of endometrial cells from women with and without endometriosis.


METHODS
Endometrial cells were isolated, cultured and treated with endometriotic or normal peritoneal fluid. Vascular endothelial growth factor-A (VEGF-A), urokinase plasminogen activator (uPA), matrix metalloproteinase-3 (MMP-3) and their inhibitors including thrombospondin-1, plasminogen activator inhibitor-1 and MMP inhibitor type 1 (TIMP-1) mRNA levels were evaluated by quantitative RT-PCR, and protein levels were quantified by ELISA.


RESULTS
Peritoneal fluid from women with endometriosis induced an increase in VEGF-A and uPA protein and VEGF-A mRNA and uPA mRNA levels in endometrial cell culture from women with (P < 0.01) and without endometriosis (P < 0.05). The highest levels of VEGF-A and uPA were observed in endometrial cell cultures from patients with endometriosis and treated with peritoneal fluid from women with endometriosis.


CONCLUSIONS
Peritoneal fluid from women with endometriosis induced more VEGF and uPA expression in endometrial cell culture from women with endometriosis than did normal peritoneal fluid. Endometrial-peritoneal interactions increased angiogenic and proteolytic factors in endometrial cells, which could contribute to the development of endometriotic lesions.
Cosín
R
R
Research Center, Hospital Universitario La Fe, Valencia, Spain.
Gilabert-Estellés
J
J
Ramón
L A
LA
Gómez-Lechón
M J
MJ
Gilabert
J
J
Chirivella
M
M
Braza-Boïls
A
A
España
F
F
Estellés
A
A
D000328:Adult; D042501:Angiogenic Proteins / Q000096:biosynthesis*; D001202:Ascitic Fluid / Q000502:physiology*; D002478:Cells, Cultured; D004715:Endometriosis / Q000378:metabolism*; D004717:Endometrium / Q000378:metabolism*; D005260:Female; D006801:Humans; D019278:Matrix Metalloproteinase 3 / Q000096:biosynthesis; D010447:Peptide Hydrolases / Q000096:biosynthesis*; D017395:Plasminogen Activator Inhibitor 1 / Q000096:biosynthesis; D019700:Thrombospondin 1 / Q000096:biosynthesis; D019715:Tissue Inhibitor of Metalloproteinase-1 / Q000096:biosynthesis; D014568:Urokinase-Type Plasminogen Activator / Q000096:biosynthesis; D042461:Vascular Endothelial Growth Factor A / Q000096:biosynthesis
D042501:Angiogenic Proteins; D017395:Plasminogen Activator Inhibitor 1; D019700:Thrombospondin 1; D019715:Tissue Inhibitor of Metalloproteinase-1; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D010447:Peptide Hydrolases; D014568:Urokinase-Type Plasminogen Activator; D019278:Matrix Metalloproteinase 3