Ensoli B, Gendelman R, Markham P, Fiorelli V, Colombini S, Raffeld M, Cafaro A, Chang H K, Brady J N, Gallo R C
Laboratory of Tumor Cell Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Nature. 1994 Oct 20;371(6499):674-80. doi: 10.1038/371674a0.
Basic fibroblast growth factor (bFGF) and human immunodeficiency virus type 1 (HIV-1) Tat protein synergize in inducing angiogenic Kaposi's sarcoma-like lesions in mice. Synergy is due to Tat, which enhances endothelial cell growth and type-IV collagenase expression in response to bFGF mimicking extracellular matrix proteins. The bFGF, extracellular Tat and Tat receptors are present in HIV-1-associated KS, which may explain the higher frequency and aggressiveness of this form compared to classical Kaposi's sarcoma where only bFGF is present.
碱性成纤维细胞生长因子（bFGF）与1型人类免疫缺陷病毒（HIV-1）的Tat蛋白协同作用，可在小鼠体内诱导出血管生成性卡波西肉瘤样病变。协同作用归因于Tat蛋白，它可增强内皮细胞生长以及IV型胶原酶的表达，从而对模仿细胞外基质蛋白的bFGF作出反应。HIV-1相关的卡波西肉瘤中存在bFGF、细胞外Tat蛋白和Tat受体，这或许可以解释为何相较于仅存在bFGF的经典卡波西肉瘤，这种形式的卡波西肉瘤具有更高的发病率和侵袭性。
