人酪氨酰-tRNA合成酶片段对血管生成的诱导作用。
Induction of angiogenesis by a fragment of human tyrosyl-tRNA synthetase.
作者信息
Wakasugi Keisuke, Slike Bonnie M, Hood John, Ewalt Karla L, Cheresh David A, Schimmel Paul
机构信息
Skaggs Institute for Chemical Biology and Department of Chemistry, The Scripps Research Institute, La Jolla, California 92037, USA.
出版信息
J Biol Chem. 2002 Jun 7;277(23):20124-6. doi: 10.1074/jbc.C200126200. Epub 2002 Apr 15.
The first step of protein synthesis is catalyzed by aminoacyl-tRNA synthetases. In addition, certain mammalian tRNA synthetases link protein synthesis to cytokine signaling pathways. In particular, human tyrosyl-tRNA synthetase (TyrRS) can be split by proteolysis into two fragments having distinct cytokine activities. One of the TyrRS fragments (mini TyrRS) contains features identical to those in CXC chemokines (like interleukin-8) that also act as angiogenic factors. Here mini TyrRS (but not full-length TyrRS) is shown to stimulate chemotaxis of endothelial cells in vitro and stimulate angiogenesis in each of two in vivo animal models. The angiogenic activity of mini TyrRS can be opposed by anti-angiogenic chemokines like IP-10. Thus, a biological fragment of human tyrosyl-tRNA synthetase links protein synthesis to regulation of angiogenesis.
蛋白质合成的第一步由氨酰-tRNA合成酶催化。此外，某些哺乳动物的tRNA合成酶将蛋白质合成与细胞因子信号通路联系起来。具体而言，人酪氨酸-tRNA合成酶（TyrRS）可通过蛋白水解作用裂解为两个具有不同细胞因子活性的片段。TyrRS片段之一（微型TyrRS）具有与CXC趋化因子（如白细胞介素-8）相同的特征，后者也作为血管生成因子发挥作用。本文显示，微型TyrRS（而非全长TyrRS）在体外可刺激内皮细胞的趋化作用，并在两种体内动物模型中均能刺激血管生成。微型TyrRS的血管生成活性可被抗血管生成趋化因子如IP-10所抑制。因此，人酪氨酸-tRNA合成酶的一个生物片段将蛋白质合成与血管生成的调节联系了起来。
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