Shih S C, Claffey K P
Departments of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
J Biol Chem. 1999 Jan 15;274(3):1359-65. doi: 10.1074/jbc.274.3.1359.
A 126-base region of human vascular endothelial growth factor (VEGF) 3'-untranslated region, which we identified as the hypoxia stability region, forms seven hypoxia-inducible RNA-protein complexes with apparent molecular masses ranging from 40 to 90 kDa in RNA-UV-cross-linking assays. In this study, we show that proteins that form the 60-kDa RNA-protein complex with the hypoxia stability region were present in both cytoplasmic and nuclear compartments. We purified the protein associated in the 60-kDa complex and identified it as heterogeneous nuclear ribonucleoprotein L (hnRNP L) by protein sequencing. Removal of hnRNP L by immunoprecipitation specifically abolished formation of the 60-kDa complex. Synthetic deoxyribonucleotide competition studies defined the RNA-binding site of hnRNP L as a 21-base-long sequence, 5'-CACCCACCCACAUACAUACAU-3'. Immunoprecipitation of hnRNP L followed by reverse transcription-polymerase chain reaction showed that hnRNP L specifically interacts with VEGF mRNA in hypoxic cells in vivo. Furthermore, when M21 cells transfected with antisense oligodeoxyribonucleotide to the hnRNP L RNA-binding site, the VEGF mRNA half-life was significantly reduced under hypoxic conditions. Thus, we propose that specific association of hnRNP L with VEGF mRNA under hypoxia may play an important role in hypoxia-induced post-transcriptional regulation of VEGF mRNA expression.
我们将人类血管内皮生长因子(VEGF)3'非翻译区的一个126个碱基的区域鉴定为缺氧稳定区,在RNA-紫外线交联试验中,该区域形成了7种缺氧诱导的RNA-蛋白质复合物,其表观分子量在40至90 kDa之间。在本研究中,我们发现与缺氧稳定区形成60 kDa RNA-蛋白质复合物的蛋白质存在于细胞质和细胞核区室中。我们纯化了与60 kDa复合物相关的蛋白质,并通过蛋白质测序将其鉴定为不均一核核糖核蛋白L(hnRNP L)。通过免疫沉淀去除hnRNP L可特异性消除60 kDa复合物的形成。合成脱氧核糖核苷酸竞争研究将hnRNP L的RNA结合位点定义为一个21个碱基长的序列,5'-CACCCACCCACAUACAUACAU-3'。对hnRNP L进行免疫沉淀后进行逆转录-聚合酶链反应,结果表明hnRNP L在体内缺氧细胞中与VEGF mRNA特异性相互作用。此外,当用针对hnRNP L RNA结合位点的反义寡脱氧核苷酸转染M21细胞时,在缺氧条件下VEGF mRNA的半衰期显著缩短。因此,我们提出缺氧条件下hnRNP L与VEGF mRNA的特异性结合可能在缺氧诱导的VEGF mRNA表达的转录后调控中起重要作用。