Problem: Aim of our study was to investigate whether TIFI, a syntetic peptide able to compete with anti-phospholipid antibodies (aPL) in the binding to endothelium, may restore aPL-inhibited endometrial angiogenesis. Methods: The protective role of TIFI was evaluated on: i) aPL-inhibited of human endometrial endothelial cells (HEEC) angiogenesis in vitro; ii) aPL-inhibited vascular endothelial growth factor (VEGF) and metalloproteases (MMPs) expression; iii) aPL-inhibited Nuclear Factor-κB (NF-κB) and Extracellular signal-Regulated Kinase (ERK) activation and (iv) angiogenesis in vivo. Results: TIFI restores in a dose-dependent manner: i) aPL-mediated inhibition of HEEC angiogenesis in vitro and in vivo (P < 0.05), ii) VEGF (P < 0.001) and MMP-2 (P < 0.05) expression and iii) NF-κB DNA binding and ERK-1/2 activation (P < 0.05) inhibited by aPL. Conclusion: Our results show for the first time the protective effects of TIFI, as represented by its ability to interfere with aPL mediated anti-angiogenic activity.
|Titolo:||Antiphospholipid Antibodies Affect Human Endometrial Angiogenesis: Protective Effect of a Synthetic Peptide (TIFI) Mimicking the Phospholipid Binding Site of β2glycoprotein I|
|Parole Chiave:||Antiphospholipid antibodies; Endometrial angiogenesis; TIFL; Antibodies, Antiphospholipid; Antibodies, Blocking; Binding Sites, Antibody; Binding, Competitive; Cells, Cultured; Endometrium; Extracellular Signal-Regulated MAP Kinases; Female; Humans; Matrix Metalloproteinase 2; NF-kappa B; Neovascularization, Pathologic; Neovascularization, Physiologic; Peptides; Phospholipids; Protein Binding; Vascular Endothelial Growth Factor A; beta 2-Glycoprotein I; Immunology; Immunology and Allergy; Obstetrics and Gynecology; Reproductive Medicine|
|Settore Scientifico Disciplinare:||Settore MED/16 - Reumatologia|
|Data di pubblicazione:||2013|
|Digital Object Identifier (DOI):||10.1111/aji.12130|
|Appare nelle tipologie:||01 - Articolo su periodico|