Nakagawa K, Zhang Y, Tsuji H, Yoshizumi M, Kasahara T, Nishimura H, Nawroth P P, Nakagawa M
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Semin Thromb Hemost. 1998;24(3):207-10. doi: 10.1055/s-2007-995843.
We report a novel function of tissue factor (TF) as an angiogenic factor in malignant and non-malignant cells and tissue. When methylcholanthrene A-induced murine fibrosarcoma (Meth-A sarcoma) was stably transfected with mouse TF (mTF) cDNA (pXT1 expression vector), its vascularization in vivo was significantly enhanced, whereas TF-antisense suppressed the vascularization and tumor growth. In vitro expression of vascular endothelial growth factor (VEGF) was enhanced with stable transfection of mTF (pcDNA3 expression vector) into a mouse fibroblast cell line (NIH3T3). Moreover, in vivo topical transfection of mTF (pcDNA3) showed an enhanced vascularization and healing in a diabetic mouse wound-healing model. This effect of TF as an angiogenic factor might be useful as an antitumor therapy against hypervascular tumors or as a novel agent against delayed wound healing.
我们报道了组织因子(TF)在恶性和非恶性细胞及组织中作为血管生成因子的一种新功能。当用小鼠TF(mTF)cDNA(pXT1表达载体)稳定转染甲基胆蒽A诱导的小鼠纤维肉瘤(Meth-A肉瘤)时,其体内血管生成显著增强,而TF反义寡核苷酸抑制了血管生成和肿瘤生长。将mTF(pcDNA3表达载体)稳定转染到小鼠成纤维细胞系(NIH3T3)中可增强血管内皮生长因子(VEGF)的体外表达。此外,在糖尿病小鼠伤口愈合模型中,mTF(pcDNA3)的体内局部转染显示血管生成增强且愈合加快。TF作为血管生成因子的这种作用可能有助于针对高血管肿瘤的抗肿瘤治疗或作为治疗伤口愈合延迟的新型药物。