PMID- 19945964 OWN - NLM STAT- MEDLINE DCOM- 20100316 LR - 20100114 IS - 1460-2350 (Electronic) IS - 0268-1161 (Linking) VI - 25 IP - 2 DP - 2010 Feb TI - Influence of peritoneal fluid on the expression of angiogenic and proteolytic factors in cultures of endometrial cells from women with endometriosis. PG - 398-405 LID - 10.1093/humrep/dep419 [doi] AB - 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. FAU - Cosin, R AU - Cosin R AD - Research Center, Hospital Universitario La Fe, Valencia, Spain. FAU - Gilabert-Estelles, J AU - Gilabert-Estelles J FAU - Ramon, L A AU - Ramon LA FAU - Gomez-Lechon, M J AU - Gomez-Lechon MJ FAU - Gilabert, J AU - Gilabert J FAU - Chirivella, M AU - Chirivella M FAU - Braza-Boils, A AU - Braza-Boils A FAU - Espana, F AU - Espana F FAU - Estelles, A AU - Estelles A LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20091126 PL - England TA - Hum Reprod JT - Human reproduction (Oxford, England) JID - 8701199 RN - 0 (Angiogenic Proteins) RN - 0 (Plasminogen Activator Inhibitor 1) RN - 0 (Thrombospondin 1) RN - 0 (Tissue Inhibitor of Metalloproteinase-1) RN - 0 (VEGFA protein, human) RN - 0 (Vascular Endothelial Growth Factor A) RN - EC 3.4.- (Peptide Hydrolases) RN - EC 3.4.21.73 (Urokinase-Type Plasminogen Activator) RN - EC 3.4.24.17 (Matrix Metalloproteinase 3) SB - IM MH - Adult MH - Angiogenic Proteins/*biosynthesis MH - Ascitic Fluid/*physiology MH - Cells, Cultured MH - Endometriosis/*metabolism MH - Endometrium/*metabolism MH - Female MH - Humans MH - Matrix Metalloproteinase 3/biosynthesis MH - Peptide Hydrolases/*biosynthesis MH - Plasminogen Activator Inhibitor 1/biosynthesis MH - Thrombospondin 1/biosynthesis MH - Tissue Inhibitor of Metalloproteinase-1/biosynthesis MH - Urokinase-Type Plasminogen Activator/biosynthesis MH - Vascular Endothelial Growth Factor A/biosynthesis EDAT- 2009/12/01 06:00 MHDA- 2010/03/17 06:00 CRDT- 2009/12/01 06:00 PHST- 2009/12/01 06:00 [entrez] PHST- 2009/12/01 06:00 [pubmed] PHST- 2010/03/17 06:00 [medline] AID - dep419 [pii] AID - 10.1093/humrep/dep419 [doi] PST - ppublish SO - Hum Reprod. 2010 Feb;25(2):398-405. doi: 10.1093/humrep/dep419. Epub 2009 Nov 26.