抗磷脂抗体影响人子宫内膜血管生成：模拟β(2)糖蛋白 I 磷脂结合位点的合成肽（TIFI）的保护作用。
Antiphospholipid antibodies affect human endometrial angiogenesis: protective effect of a synthetic peptide (TIFI) mimicking the phospholipid binding site of β(2) glycoprotein I.
机构信息
Department of Obstetrics and Gynecology, Università Cattolica del Sacro Cuore, Rome, Italy.
出版信息
Am J Reprod Immunol. 2013 Oct;70(4):299-308. doi: 10.1111/aji.12130. Epub 2013 May 7.
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.
问题
我们的研究目的是探讨 TIFI，一种能够与抗磷脂抗体（aPL）竞争结合内皮细胞的合成肽，是否可以恢复 aPL 抑制的子宫内膜血管生成。
方法
评估 TIFI 在以下方面的保护作用：i）体外 aPL 抑制的人子宫内膜内皮细胞（HEEC）血管生成；ii）aPL 抑制的血管内皮生长因子（VEGF）和金属蛋白酶（MMPs）表达；iii）aPL 抑制核因子-κB（NF-κB）和细胞外信号调节激酶（ERK）的激活；iv）体内血管生成。
结果
TIFI 以剂量依赖的方式恢复：i）体外和体内 aPL 介导的 HEEC 血管生成抑制（P < 0.05），ii）VEGF（P < 0.001）和 MMP-2（P < 0.05）表达，以及 iii）NF-κB DNA 结合和 ERK-1/2 激活（P < 0.05）被 aPL 抑制。
结论
我们的结果首次表明 TIFI 具有保护作用，表现在其能够干扰 aPL 介导的抗血管生成活性。
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