Yamazaki Yasuo, Nakano Yuta, Imamura Takahisa, Morita Takashi
Department of Biochemistry, Meiji Pharmaceutical University, 2-522-1 Noshio, Kiyose, Tokyo 204-8588, Japan.
Biochem Biophys Res Commun. 2007 Apr 13;355(3):693-9. doi: 10.1016/j.bbrc.2007.02.038. Epub 2007 Feb 15.
VEGF165 is a key regulator of angiogenesis and a potent vascular permeability factor. Using snake venom proteins as tools, we demonstrate the enhanced vascular leakage of VEGF by KDR-binding proteins. The snake venom-derived KDR-specific VEGF, vammin, potently enhanced vascular leakage compared with other known permeability-enhancing factors including VEGF165, while KDR-bp from snake venom, a KDR antagonist of endothelial cell growth was a very weak permeability enhancer. Unexpectedly when co-administrated, KDR-bp synergistically enhanced either vammin or VEGF165-stimulated vascular leakage, despite its antagonistic effect on cell growth. This augmenting effect was specifically observed in the combined administration of KDR-bp with either VEGF165 or vammin, but not other combination of known permeability-enhancing factors. We further demonstrated a similar increased vascular leakage by the combined administration of VEGF165 and TIMP-3, the only known endogenous antagonist of KDR. Our findings implicate TIMP-3 as a critical player in the vascular leakage-enhancing effect of VEGF165 in vivo.
血管内皮生长因子165(VEGF165)是血管生成的关键调节因子,也是一种强效的血管通透性因子。我们以蛇毒蛋白作为工具,证明了与激酶插入区受体(KDR)结合的蛋白可增强VEGF引起的血管渗漏。源自蛇毒的KDR特异性VEGF——vammin,与包括VEGF165在内的其他已知通透性增强因子相比,能显著增强血管渗漏,而蛇毒来源的KDR结合蛋白(KDR-bp),一种内皮细胞生长的KDR拮抗剂,却是非常弱的通透性增强剂。出乎意料的是,共同给药时,尽管KDR-bp对细胞生长有拮抗作用,但它能协同增强vammin或VEGF165刺激引起的血管渗漏。这种增强效应在KDR-bp与VEGF165或vammin联合给药时特异性观察到,而在已知通透性增强因子的其他组合中未观察到。我们进一步证明,联合给予VEGF165和组织金属蛋白酶抑制剂3(TIMP-3),唯一已知的KDR内源性拮抗剂,也会出现类似的血管渗漏增加。我们的研究结果表明,TIMP-3是VEGF165在体内增强血管渗漏作用中的关键参与者。