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鉴定触珠蛋白为系统性血管炎患者血清中的一种血管生成因子。

Identification of haptoglobin as an angiogenic factor in sera from patients with systemic vasculitis.

作者信息

Cid M C, Grant D S, Hoffman G S, Auerbach R, Fauci A S, Kleinman H K

机构信息

Laboratory of Immunoregulation, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892.

出版信息

J Clin Invest. 1993 Mar;91(3):977-85. doi: 10.1172/JCI116319.

DOI:10.1172/JCI116319
PMID:7680672
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC288050/
Abstract

Angiogenesis is an important process in chronic inflammatory diseases. We observed that sera from patients with systemic vasculitis stimulated angiogenesis in an in vitro model using human umbilical vein endothelial cells cultured on a basement membrane (Matrigel) substrate. After 40% ammonium sulfate precipitation, angiogenic activity remained in the low molecular weight fraction and could be inactivated by heat. SDS-page of serum FPLC fractions exhibiting maximal angiogenic activity demonstrated two prominent species of 45 and 16-20 kD in patients' sera. These bands were much less apparent in sera obtained from control subjects. Amino-terminal sequencing of the 45-kD protein demonstrated that it was haptoglobin. Purified haptoglobin stimulated angiogenesis in a dose-dependent manner. The angiogenic activity of vasculitis patients' sera was partially inhibited by an antihaptoglobin antibody. Furthermore, serum haptoglobin levels in vasculitis patients correlated both with disease and angiogenic activity. Haptoglobin angiogenic activity was confirmed in two in vivo models using an implanted disc and a subcutaneous injection of basement membrane. Stimulation of angiogenesis is a newly recognized biological function of haptoglobin. The increased levels of haptoglobin found in chronic inflammatory conditions may play an important role in tissue repair. In systemic vasculitis, haptoglobin might also compensate for ischemia by promoting development of collateral vessels.

摘要

血管生成是慢性炎症性疾病中的一个重要过程。我们观察到，在使用培养于基底膜（基质胶）底物上的人脐静脉内皮细胞的体外模型中，系统性血管炎患者的血清可刺激血管生成。经40%硫酸铵沉淀后，血管生成活性保留在低分子量组分中，且可被加热灭活。对表现出最大血管生成活性的血清快速蛋白质液相色谱（FPLC）组分进行十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-page）分析，结果显示患者血清中有两种明显的条带，分子量分别为45 kD和16 - 20 kD。在对照受试者的血清中，这些条带则不那么明显。对45-kD蛋白进行氨基末端测序表明它是触珠蛋白。纯化的触珠蛋白以剂量依赖的方式刺激血管生成。血管炎患者血清的血管生成活性被抗触珠蛋白抗体部分抑制。此外，血管炎患者的血清触珠蛋白水平与疾病及血管生成活性均相关。在使用植入盘和皮下注射基底膜的两种体内模型中证实了触珠蛋白的血管生成活性。刺激血管生成是触珠蛋白一种新发现的生物学功能。在慢性炎症状态下发现的触珠蛋白水平升高可能在组织修复中起重要作用。在系统性血管炎中，触珠蛋白还可能通过促进侧支血管的发育来补偿局部缺血。

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急性相蛋白的新作用：局部产生是哺乳动物细胞古老而普遍的应激反应系统。
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