title: FGF-1 and S100A13 possibly contribute to angiogenesis in endometriosis.
abstract: Endometriosis is referred often as an angiogenic disease. The pivotal role of angiogenesis in the pathophysiology of this disease has been confirmed by many studies. This process has several steps, and VEGF is probably the most important in its initiation. There are others involved in its continuation and maintenance of the tight balance between a quiescent and activated blood vessel state. In the process of formation of new blood capillaries and arterioles, many different factors are involved in sometimes distinct pathways. Such factors are TGF-beta and endoglin--the latter being one of the main modulators of the TGF-beta signaling pathway. Endoglin is now not only established as a marker of active neo-angiogenesis and activated endothelium, but also turns to be an active player in the very process of endometriotic angiogenesis. Its signaling pathway of hypoxic activation is tightly interconnected with that of VEGF, and also some of the FGFs. FGF-1 and S100A13 are members of two distinct families of proteins -- the FGFs, growth and angiogenic factors, and that of the S100 proteins, -- Ca(2+)-binding proteins involved in cell function regulation, motility and signaling. These two particular members are quite unique in having no signal peptide sequence and being involved in common export pathway. Our hypothesis is that these two factors are involved in vascular remodeling in endometriotic angiogenesis, playing a role in vascular wall formation and migration of endothelial cells (ECs) and vascular smooth muscle cells (VSMCs). We believe also that endoglin is tightly involved in the new arteriolar formation in endometriosis, being expressed in VSMCs but not on the ECs of the middle-sized vessels.
authors.affiliation: Molecular Immunology Department, Institute of Biology and Immunology of Reproduction "Akad. K. Bratanov", Bulgarian Academy of Sciences, Sofia 1113, 73, Tsarigrdasko shosse blvd., Bulgaria.
authors.forename: Soren
authors.initials: S
authors.lastname: Hayrabedyan
authors.forename: Stanimir
authors.initials: S
authors.lastname: Kyurkchiev
authors.forename: Ivan
authors.initials: I
authors.lastname: Kehayov
mesh_terms: D000818:Animals; D015703:Antigens, CD; D002465:Cell Movement; D000071063:Endoglin; D004715:Endometriosis / Q000378:metabolism* / Q000473:pathology; D042783:Endothelial Cells / Q000378:metabolism*; D005260:Female; D016220:Fibroblast Growth Factor 1 / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D000860:Hypoxia / Q000378:metabolism / Q000473:pathology; D009389:Neovascularization, Pathologic / Q000378:metabolism* / Q000473:pathology; D011956:Receptors, Cell Surface; D009418:S100 Proteins / Q000378:metabolism*; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000378:metabolism; D019010:Vascular Cell Adhesion Molecule-1 / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; D011956:Receptors, Cell Surface; D009418:S100 Proteins; C511523:S100A13 protein, human; D016212:Transforming Growth Factor beta; C467484:VEGFA protein, human; D019010:Vascular Cell Adhesion Molecule-1; D042461:Vascular Endothelial Growth Factor A; D016220:Fibroblast Growth Factor 1