Expression of the Fibrinolytic Components in Endometriosis

Endometriosis is a benign gynaecologic disease defined as the presence of endometrial tissue outside the uterus. This tissue has the ability to implant at ectopic sites, such as ovary and peritoneum, where a local extracellular proteolysis might take place. An altered expression of several components of the fibrinolytic system in the endometrium and peritoneal fluid of women with the disease has been suggested as a key factor in the establishment of the endometriotic lesions. There is evidence of increased fibrinolytic activity in the eutopic endometrium of these women, resulting in endometrial fragments with a high potential to degrade the extracellular matrix and facilitate implantation. Proteolytic status is determined by the imbalance between plasminogen activators and plasminogen activator inhibitors, which are expressed differently depending on the type of lesion considered and the stage of the disease. The aim of the present study is to review the expression of the plasminogen activator system in endometriosis, and to consider the clinical implications and the possible further research efforts in this disease.

[1]  J. Gilabert-Estellés,et al.  Plasminogen activators and plasminogen activator inhibitors in endometriosis. , 2005, Frontiers in bioscience : a journal and virtual library.

[2]  A. Bergqvist,et al.  Basal release of urokinase plasminogen activator, plasminogen activator inhibitor-1, and soluble plasminogen activator receptor from separated and cultured endometriotic and endometrial stromal and epithelial cells. , 2005, Fertility and sterility.

[3]  A. Bergqvist,et al.  In situ localization of mRNA for the fibrinolytic factors uPA, PAI-1 and uPAR in endometriotic and endometrial tissue. , 2004, Molecular human reproduction.

[4]  N. Terakawa,et al.  Hepatocyte growth factor/Met system promotes endometrial and endometriotic stromal cell invasion via autocrine and paracrine pathways. , 2004, The Journal of clinical endocrinology and metabolism.

[5]  G. Edelstam,et al.  Fibrinolysis in the Peritoneal Fluid During Adhesions, Endometriosis and Ongoing Pelvic Inflammatory Disease , 1998, Inflammation.

[6]  M. Koutsilieris,et al.  Urokinase‐Type Plasminogen Activator and Insulin‐Like Growth Factor‐Binding Protein 3 mRNA Expression in Endometriotic Lesions and Eutopic Endometrium , 2003 .

[7]  J. Gilabert-Estellés,et al.  Expression of several components of the plasminogen activator and matrix metalloproteinase systems in endometriosis. , 2003, Human reproduction.

[8]  A. Bergqvist,et al.  Impact of Epidermal Growth Factor and Transforming Growth Factor Beta-1 on the Release of Fibrinolytic Factors from Cultured Endometrial and Ovarian Endometriotic Stromal Cells , 2003, Gynecologic and Obstetric Investigation.

[9]  M. Koutsilieris,et al.  Urokinase-type plasminogen activator and insulin-like growth factor-binding protein 3 mRNA expression in endometriotic lesions and eutopic endometrium: implications for the pathophysiology of endometriosis. , 2003, Annals of the New York Academy of Sciences.

[10]  F. España,et al.  Quantitative real-time reverse transcription-PCR assay for urokinase plasminogen activator, plasminogen activator inhibitor type 1, and tissue metalloproteinase inhibitor type 1 gene expressions in primary breast cancer. , 2002, Clinical chemistry.

[11]  A. Bergqvist,et al.  Effects of hormones on uPA, PAI‐1 and suPAR from cultured endometrial and ovarian endometriotic stromal cells , 2002, Acta obstetricia et gynecologica Scandinavica.

[12]  H. Stefánsson,et al.  Genetic factors contribute to the risk of developing endometriosis. , 2002, Human reproduction.

[13]  N. Garrido,et al.  Endometrial Quality in Infertile Women with Endometriosis , 2001, Annals of the New York Academy of Sciences.

[14]  K. L. Sharpe-Timms,et al.  Endometrial Anomalies in Women with Endometriosis , 2001, Annals of the New York Academy of Sciences.

[15]  A. Krüger,et al.  Clinical Relevance of the Plasminogen Activator Inhibitor Type1 – a Multifaceted Proteolytic Factor , 2001, Oncology Research and Treatment.

[16]  Hiroshi Kobayashi.  Invasive Capacity of Heterotopic Endometrium , 2000, Gynecologic and Obstetric Investigation.

[17]  S. Manoir,et al.  Genetic abnormalities detected by comparative genomic hybridization in a human endometriosis-derived cell line. , 2000, Molecular human reproduction.

[18]  D. Edwards,et al.  Cellular mechanisms for focal proteolysis and the regulation of the microenvironment , 2000 .

[19]  P. Andreasen,et al.  The plasminogen activation system in tumor growth, invasion, and metastasis , 2000, Cellular and Molecular Life Sciences CMLS.

[20]  J. Gilabert,et al.  Inhibition of human sperm–zona‐free hamster oocyte binding and penetration by protein C inhibitor , 1999, Andrologia.

[21]  F. España,et al.  Two Distinct Urokinase-Serpin Interactions Regulate the Initiation of Cell Surface-associated Plasminogen Activation* , 1999, The Journal of Biological Chemistry.

[22]  D. Barlow,et al.  Pathogenesis of Endometriosis: The Role of Peritoneal Fluid , 1999, Gynecologic and Obstetric Investigation.

[23]  A. Bergqvist,et al.  Fibrinolytic factors in endometriotic tissue, endometrium, peritoneal fluid, and plasma from women with endometriosis and in endometrium and peritoneal fluid from healthy women. , 1998, Fertility and sterility.

[24]  L. Giudice,et al.  Status of current research on endometriosis. , 1998, The Journal of reproductive medicine.

[25]  S. Prifti,et al.  Soluble urokinase-type plasminogen activator receptor is over-expressed in uterine endometrium from women with endometriosis. , 1997, Molecular human reproduction.

[26]  J. Gilabert,et al.  Decreased Expression of PAI-2 mRNA and Protein in Pregnancies Complicated with Intrauterine Fetal Growth Retardation , 1996, Thrombosis and Haemostasis.

[27]  Michael V. Doyle,et al.  Regulation of Integrin Function by the Urokinase Receptor , 1996, Science.

[28]  A. Mazar,et al.  Single-chain urokinase-type plasminogen activator bound to its receptor is relatively resistant to plasminogen activator inhibitor type 1. , 1996, Blood.

[29]  J. Gilabert,et al.  Fibrinolytic system and reproductive process with special reference to fibrinolytic failure in pre-eclampsia. , 1995, Human reproduction.

[30]  M. Baker,et al.  Biological and clinical aspects of plasminogen activator inhibitor type 2. , 1995, Blood.

[31]  Y. Eguchi,et al.  Altered expression of plasminogen activator inhibitor type 1 in placentas from pregnant women with preeclampsia and/or intrauterine fetal growth retardation. , 1994, Blood.

[32]  J. Griffin,et al.  Evidence for the Regulation of Urokinase and Tissue Type Plasminogen Activators by the Serpin, Protein C Inhibitor, in Semen and Blood Plasma , 1993, Thrombosis and Haemostasis.

[33]  M. Nisolle,et al.  Morphometric study of the stromal vascularization in peritoneal endometriosis. , 1993, Fertility and sterility.

[34]  G. Dunselman,et al.  Early endometriosis invades the extracellular matrix. , 1992, Fertility and sterility.

[35]  G. Dooijewaard,et al.  Peritoneal Fluid and Plasma Fibrinolytic Activity in Women with Pelvic Inflammatory Disease , 1992, Thrombosis and Haemostasis.

[36]  J. Gilabert,et al.  Functionally active protein C inhibitor/plasminogen activator inhibitor-3 (PCI/PAI-3) is secreted in seminal vesicles, occurs at high concentrations in human seminal plasma and complexes with prostate-specific antigen. , 1991, Thrombosis research.

[37]  D. Loskutoff.  Regulation of PAI-1 gene expression , 1991 .

[38]  P. Jap,et al.  Endometrial epithelial cells in peritoneal fluid during the early follicular phase. , 1991, Fertility and sterility.

[39]  G. Dunselman,et al.  Fibrinolytic properties of peritoneal fluid in endometriosis. , 1988, Gynecologic and obstetric investigation.

[40]  J. Griffin,et al.  Immunological identity of heparin-dependent plasma and urinary protein C inhibitor and plasminogen activator inhibitor-3. , 1987, The Journal of biological chemistry.

[41]  J. Mimuro,et al.  Extracellular matrix of cultured bovine aortic endothelial cells contains functionally active type 1 plasminogen activator inhibitor. , 1987, Blood.

[42]  W. Gibbons,et al.  Peritoneal fluid plasminogen activator activity in endometriosis and pelvic adhesive disease. , 1985, Fertility and sterility.

[43]  B. Åstedt,et al.  Plasminogen activators in endometriosis , 1984, Acta obstetricia et gynecologica Scandinavica. Supplement.

[44]  B. Åstedt,et al.  Occurrence of both urokinase and tissue plasminogen activator in the human endometrium. , 1983, Contraception.

[45]  B. Casslén,et al.  Effect of IUD on urokinase-like immunoreactivity and plasminogen activators in human uterine fluid. , 1981, Contraception.