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Midkine, a cytokine that inhibits HIV infection by binding to the cell surface expressed nucleolin

机译：Midkine，一种通过与细胞表面表达的核仁结合而抑制HIV感染的细胞因子

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摘要

The growth factor midkine (MK) is a cytokine that inhibits HIV infection in cell cultures in an autocrine and paracrine manner by blocking the attachment of HIV particles to permissive cells. MK mRNA is systematically expressed in adult peripheral blood lymphocytes from healthy donors, while its expression becomes markedly but transiently increased upon in vitro treatment of lymphocytes with IL-2 or IFN-γ and activation of T lymphocytes by PHA or through the engagement of the CD28 antigen. The binding of MK to cells occurs specifically at a high and a low affinity binding site. This low affinity-binding site is the cell-surface expressed nucleolin, which is implicated in the mechanism of the initial attachment of HIV particles to cells. Accordingly, the nucleolin-binding HB-19 pseudopeptide has no effect on the MK binding to the high affinity binding site, whereas it prevents the binding of MK to the low affinity binding site, thus suggesting the low affinity receptor of MK is the cell-surface-expressed nucleolin. Confocal immunofluorescence laser microscopy revealed the colocalization of MK and the cell-surface-expressed nucleolin at distinct spots. The use of various deletion constructs of nucleolin then indicates that the extreme C-terminal end of nucleolin, containing repeats of the amino acid motif RGG, as the domain that binds MK. The specific binding of MK to the surface nucleolin is independent of heparan sulfate and chondroitin sulfate proteoglycans. After binding to cells, MK enters cells by an active process in which nucleolin and lipid rafts appear to be implicated. The potent and the distinct anti-HIV action of MK along with its enhanced expression in lymphocytes by various physiological stimuli, point out that MK is a cytokine that could be involved in HIV pathogenesis.
机译：生长因子中期因子（MK）是一种细胞因子，可通过阻止HIV颗粒附着在允许的细胞上，以自分泌和旁分泌的方式抑制细胞培养物中的HIV感染。 MK mRNA在健康捐献者的成人外周血淋巴细胞中系统表达，而在用IL-2或IFN-γ体外处理淋巴细胞并通过PHA或通过CD28激活T淋巴细胞后，MK mRNA的表达明显但短暂增加。抗原。 MK与细胞的结合特别发生在高和低亲和力结合位点。这种低亲和力结合位点是细胞表面表达的核仁素，与HIV颗粒最初附着于细胞的机制有关。因此，与核仁素结合的HB-19假肽对MK与高亲和力结合位点的结合没有影响，而它阻止了MK与低亲和力结合位点的结合，因此表明MK的低亲和力受体是细胞-表面表达的核仁蛋白。共聚焦免疫荧光激光显微术揭示了MK和细胞表面表达的核仁素在不同点的共定位。然后，使用核仁蛋白的各种缺失构建体表明核仁蛋白的C末端极端，该末端含有氨基酸基序RGG的重复，作为结合MK的域。 MK与表面核仁素的特异性结合不依赖于硫酸乙酰肝素和硫酸软骨素蛋白聚糖。与细胞结合后，MK通过活跃的过程进入细胞，其中涉及核仁素和脂质筏。 MK的强大而独特的抗HIV作用，以及各种生理刺激在淋巴细胞中的增强表达，指出MK是一种可能参与HIV发病机制的细胞因子。

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  • 来源
    《Cell Research》 |2006年第2期|p.174-181|共8页
  • 作者

    Ara G Hovanessian;

  • 作者单位

    UPR 2228 CNRS, UFR Biomedicale-Universite Rene Descartes, 45 rue des Saints Peres, 75270 Paris Cedex 6, France;

  • 收录信息 美国《科学引文索引》(SCI);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    HIV; Midkine; surface nucleolin; cytokine;

    机译：HIV;Midkine;表面核仁蛋白;细胞因子;

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