Endoglin (cd105) and S100A13 as markers of active angiogenesis in endometriosis.

نویسندگان

  • Soren Hayrabedyan
  • Stanimir Kyurkchiev
  • Ivan Kehayov
چکیده

The aim of the present study was to evaluate the expression of the neo-angiogenic marker endoglin and its localization in tissues of normal and endometriotic patients as well as to compare it with one new angiogenic marker candidate - S100A13. Human recombinant S100A13 and endoglin 35mer synthetic peptide of the intracellular domain were used for the production of rabbit polyclonal antisera. The antisera were characterized for specificity, using immunoenzyme assay (ELISA), Western blot and immunohistochemistry. Formalin-fixed, paraffin-embedded tissue sections from normal endometrium, adenomyosis, ovarian endometriosis, eutopic endometrium from different endometriotic specimens were tested by immunohistochemistry. No endoglin specific staining was observed on the microvessels of the normal endometrium. In adenomyosis and ovarian endometriosis, the expression pattern was different - endoglin was expressed in all microvessels, with an even stronger expression in the myometrial compartment. Weak endoglin-positive staining was detected in the microvessels of eutopic endometrium specimens from different endometriosis cases. In comparison to endoglin, S100A13 exhibited a moderate expression in endometrial glands of normal endometrium, but strong expression in endometriotic specimens. No S100A13 extensive staining of the microvessels was observed in normal endometrium, while in endometriosis, it exhibited very intense staining in microvascular endothelia and less intense in the perivascular area of middle to large-sized vessels. This study for the first time shows over-expression of S100A13 in endometriosis. These data show that the expression of endoglin and S100A13 corresponds to the activation of the endothelial cells in the process of endometriotic angiogenesis, suggesting a beneficial role for these two molecules as markers for actively progressing endometriotic process.

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عنوان ژورنال:
  • Reproductive biology

دوره 5 1  شماره 

صفحات  -

تاریخ انتشار 2005