人类免疫缺陷病毒1型外壳蛋白gp120调节神经祖细胞中CXCR4介导的信号传导。
The HIV-1 coat protein gp120 regulates CXCR4-mediated signaling in neural progenitor cells.
作者信息
Tran Phuong B, Ren Dongjun, Miller Richard J
机构信息
Department of Molecular Pharmacology and Biological Chemistry, Feinberg School of Medicine, Northwestern University, MPBC, m/c S215 W8-296, 303 E Chicago Ave., Chicago, IL 60611, USA.
出版信息
J Neuroimmunol. 2005 Mar;160(1-2):68-76. doi: 10.1016/j.jneuroim.2004.11.001. Epub 2004 Dec 28.
Abstract
We demonstrate that hCD4-primed gp120IIIB interacts with CXCR4 receptors expressed by postnatal mouse neural progenitor cells and elicits robust Ca(2+) signals. The chemokine SDF-1 acted as a chemoattractant and a mitogenic stimulus for these neural progenitor cells. Although hCD4/gp120 was not able to produce chemoattraction or increase proliferation, it completely blocked the ability of SDF-1 to produce these effects. Thus, gp120 can act both as an agonist and de facto antagonist of CXCR4-mediated signaling in neural progenitor cells. It is possible that the ability of hCD4/gp120 to block SDF-1 signaling in neural progenitors may contribute to the neuropathological effects of HIV-1.
摘要
我们证明，经hCD4预处理的gp120IIIB与出生后小鼠神经祖细胞表达的CXCR4受体相互作用，并引发强烈的Ca(2+)信号。趋化因子SDF-1对这些神经祖细胞起到化学引诱剂和促有丝分裂刺激物的作用。尽管hCD4/gp120无法产生化学引诱或增加增殖作用，但它完全阻断了SDF-1产生这些效应的能力。因此，gp120在神经祖细胞中既可以作为CXCR4介导信号传导的激动剂，也可以作为事实上的拮抗剂。hCD4/gp120阻断神经祖细胞中SDF-1信号传导的能力可能导致了HIV-1的神经病理学效应。
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