Purpose: Neo-angiogenesis is necessary for adhesion and invasiveness of endometriotic lesions
in women affected by endometriosis. VEGF is one of the major components of angiogenesis and
is part of the major pathway TF-PAR-2-VEGF that leads to neo-angiogenesis. SP1 is a
transcriptional factor that has lately been studied for its crucial role in angiogenesis, via
a distinct pathway. We hypothesize that by blocking angiogenetic pathways we can repress
endometriotic lesions. GnRH-agonists are routinely used, especially pre-operatively, in
endometriosis. It would be interesting to clarify which angiogenetic pathways are affected
and pave the way for further research over anti-angiogenetic effects on endometriosis.
Methods: We used qRT-PCR to study mRNA expression levels of TF, PAR-2, VEGF and SP1 in
endometriotic tissues of women who underwent surgery for endometriosis and received GnRH-a
[leuprolide acetate] preoperatively.