NERVE GROWTH FACTOR ACTS THROUGH THE TRKA RECEPTOR TO PROTECT SENSORY NEURONS FROM THE DAMAGING EFFECTS OF THE HIV-1 VIRAL PROTEIN, VPR

C. A. WEBBER; J. SALAME; G.-L. S. LUU; S. ACHARJEE; A. RUANGKITTISAKUL

首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >NERVE GROWTH FACTOR ACTS THROUGH THE TRKA RECEPTOR TO PROTECT SENSORY NEURONS FROM THE DAMAGING EFFECTS OF THE HIV-1 VIRAL PROTEIN, VPR

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NERVE GROWTH FACTOR ACTS THROUGH THE TRKA RECEPTOR TO PROTECT SENSORY NEURONS FROM THE DAMAGING EFFECTS OF THE HIV-1 VIRAL PROTEIN, VPR

机译：神经生长因子通过TRKA受体保护HIV-1病毒蛋白（VPR）的破坏作用来保护感觉神经元

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Distal sensory polyneuropathy (DSP) with associated neuropathic pain is the most common neurological disorder affecting patients with human immunodeficiency virus/acquired immunodeficiency syndrome (HIV/AIDS). Viral protein R (Vpr) is a neurotoxic protein encoded by HIV-1 and secreted by infected macrophages. Vpr reduces neuronal viability, increases cytosolic calcium and membrane excitability of cultured dorsal root ganglion (DRG) sensory neurons, and is associated with mechanical allo-dynia in vivo. A clinical trial with HIV/AIDS patients demonstrated that nerve growth factor (NGF) reduced the severity of DSP-associated neuropathic pain, a problem linked to damage to small diameter, potentially NGF-responsive fibers. Herein, the actions of NGF were investigated in our Vpr model of DSP and we demonstrated that NGF significantly protected sensory neurons from the effects of Vpr. Footpads of immunodeficient Vpr transgenic (vpr/RAG1-/-) mice displayed allodynia (p < 0.05), diminished epidermal-innervation (p < 0.01) and reduced NGF mRNA expression (p < 0.001) compared to immunodeficient (wildtype/RAGI-/-) littermate control mice.

机译：伴有神经性疼痛的远端感觉性多发性神经病（DSP）是影响人类免疫缺陷病毒/后天免疫缺陷综合症（HIV / AIDS）患者的最常见神经系统疾病。病毒蛋白R（Vpr）是一种由HIV-1编码并由感染的巨噬细胞分泌的神经毒性蛋白。 Vpr降低神经元生存力，增加培养的背根神经节（DRG）感觉神经元的胞质钙和膜兴奋性，并与体内机械性异力性肌痛相关。一项针对HIV / AIDS患者的临床试验表明，神经生长因子（NGF）可以降低与DSP相关的神经性疼痛的严重程度，这是与小直径，可能对NGF敏感的纤维受损相关的问题。在本文中，在我们的DSP Vpr模型中研究了NGF的作用，并证明了NGF可以有效地保护感觉神经元免受Vpr的影响。免疫缺陷型Vpr转基因（vpr / RAG1-/-）小鼠的脚垫与免疫缺陷型（wildtype / RAGI- / -）同窝对照小鼠。

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《Neuroscience: An International Journal under the Editorial Direction of IBRO》 |2013年第null期|共14页
作者
C. A. WEBBER; J. SALAME; G.-L. S. LUU; S. ACHARJEE; A. RUANGKITTISAKUL;
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neuropathic pain; dorsal root ganglion; human immunodeficiency virus (HIV); viral protein R (Vpr); nerve growth factor (NGF); tropomyosin-related kinase A (TrkA).;

机译：神经性疼痛;背根神经节;人免疫缺陷病毒（HIV）;病毒蛋白R（Vpr）;神经生长因子（NGF）;原肌球蛋白相关激酶A（TrkA）。;

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1. NERVE GROWTH FACTOR ACTS THROUGH THE TRKA RECEPTOR TO PROTECT SENSORY NEURONS FROM THE DAMAGING EFFECTS OF THE HIV-1 VIRAL PROTEIN, VPR [J] . C. A. WEBBER, J. SALAME, G.-L. S. LUU, Neuroscience: An International Journal under the Editorial Direction of IBRO . 2013,第Null期

机译：神经生长因子通过TRKA受体保护HIV-1病毒蛋白（VPR）的破坏作用来保护感觉神经元
2. Nerve growth factor regulates substance P in adult sensory neurons through both TrkA and p75 receptors. [J] . Skoff AM, Adler JE Experimental Neurology . 2006,第2期

机译：神经生长因子通过TrkA和p75受体调节成人感觉神经元中的P物质。
3. Protective effect of HSV-mediated gene transfer of nerve growth factor in pyridoxine neuropathy demonstrates functional activity of trkA receptors in large sensory neurons of adult animals. [J] . Chattopadhyay M, Goss J, Lacomis D, The European Journal of Neuroscience . 2003,第4期

机译：HSV介导的神经生长因子基因转移在吡ido醇神经病中的保护作用证明了成年动物大感觉神经元中trkA受体的功能活性。
4. HIV Viral Protein R (Vpr)-Derived Peptides Designed as HIV-1 Integrase Photoaffinity Ligands [C] . Xue Zhi Zhao, Mathieu Metifiot, Kasthuraiah Maddali American Peptide Symposium . 2013

机译：艾滋病毒病毒蛋白R（VPR）设计为HIV-1整合酶光亚蜜配体的肽
5. Factors influencing function: Activation of antigen presenting cells by the cholera toxin B-subunit, and regulation of the cholinergic phenotype in nerve growth factor receptor-positive basal forebrain cholinergic neurons by bone morphogenetic protein 9. [D] . Schnitzler, Aletta Christina. 2007

机译：影响功能的因素：霍乱毒素B亚基激活抗原呈递细胞，并通过骨形态发生蛋白9调节神经生长因子受体阳性基底前脑胆碱能神经元的胆碱能表型。
6. Nerve growth factor acts through the TrkA receptor to protect sensory neurons from the damaging effects of the HIV-1 viral protein Vpr [O] . Christine A. Webber, Jihan Salame, Gia-Linh S. Luu, -1

机译：神经生长因子通过TrkA受体起作用以保护感觉神经元免受HIV-1病毒蛋白Vpr的破坏作用
7. Nerve growth factor acts through the TrkA receptor to protect sensory neurons from the damaging effects of the HIV-1 viral protein, Vpr [O] . C.A. Webber, J. Salame, G.-L.S. Luu, 2013

机译：神经生长因子通过Trka受体作用，保护感觉神经元免受HIV-1病毒蛋白的破坏性影响，VPR
8. Human Immunodeficiency Virus Type 1 (HIV-1) Viral Protein R (Vpr)- Mediated Cell Cycle Arrest: An Analysis of Current Mechanistic Models [R] . Sercovich, M. J. 2006

机译：人类免疫缺陷病毒1型（HIV-1）病毒蛋白R（Vpr） - 介导的细胞周期逮捕：当前机制模型的分析

NERVE GROWTH FACTOR ACTS THROUGH THE TRKA RECEPTOR TO PROTECT SENSORY NEURONS FROM THE DAMAGING EFFECTS OF THE HIV-1 VIRAL PROTEIN, VPR

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