Department of Internal Medicine, Centre for Molecular Biotechnology, University of Turin, Italy.
Microvasc Res. 2009 Dec;78(3):272-7. doi: 10.1016/j.mvr.2009.07.001. Epub 2009 Jul 23.
Endothelial cell proliferation and the formation of new vessels are strictly regulated by angiogenic factors (e.g., VEGF) that induce the activation of signal transduction pathways controlled by calcium dynamics. Using in vitro and in vivo experiments, we investigated the effect of calcium trifluoroacetate (CaTFAc), a complex, poorly dissociated salt that is characterized by its low toxicity, on angiogenesis. In vitro, CaTFAc inhibited VEGF-induced effects on endothelial cell proliferation. In two in vivo models of angiogenesis, a Matrigel plug in mice and a chick embryo chorioallantoic membrane, CaTFAc inhibited the VEGF-induced formation of new vessels. The exact mechanism of action is still under investigation, but in vitro experiments demonstrate that CaTFAc induced a reversible increase in the levels of intracellular calcium under basal conditions and prevented calcium signaling induced by VEGF. These results are the first to suggest that CaTFAc may be useful for the treatment of diseases caused by enhanced angiogenesis.
内皮细胞增殖和新血管的形成受到血管生成因子（如 VEGF）的严格调节，这些因子诱导受钙动态控制的信号转导途径的激活。我们使用体外和体内实验研究了钙三氟乙酸盐（CaTFAc）对血管生成的影响。CaTFAc 是一种复杂的、不易解离的盐，其特点是毒性低，对内皮细胞增殖有抑制作用。在两种血管生成的体内模型中，即小鼠的 Matrigel plugs 和鸡胚绒毛尿囊膜中，CaTFAc 抑制了 VEGF 诱导的新血管形成。其确切的作用机制仍在研究中，但体外实验表明，CaTFAc 在基础条件下诱导细胞内钙水平的可逆增加，并阻止 VEGF 诱导的钙信号。这些结果首次表明，CaTFAc 可能对治疗因血管生成增强而引起的疾病有用。
