Cocaine-induced HIV-1 expression in microglia involves sigma-1 receptors and transfonning growth factor-β1

Cocaine-induced HIV-1 expression in microglia involves sigma-1 receptors and transfonning growth factor-β1
复制标题

DOI:
10.1016/j.intimp.2005.12.005
复制
发表时间:
2006-06-01
影响因子:
5.6
通讯作者:
Peterson, Phillip K.
Peterson, Phillip K.
中科院分区:
医学2区
文献类型:
--
作者:
Gekker, Genya;hu, Sxian Hu;Peterson, Phillip K.

文献摘要

被引文献

相似文献

已知可卡因的神经药理特性与Sigma-1受体的激活有关。可卡因还被证明改变了单核吞噬细胞中细胞因子的产生和HIV-1的表达,包括小胶质细胞。本研究验证了一种假设,即Sigma-L受体和转化生长因子-β1参与了可卡因诱导的小胶质细胞培养中HIV-1表达的上调。用可卡因处理小胶质细胞,通过测量培养上清液中的p24抗原水平来评估病毒表达的浓度依赖性增加。用Sigma-L受体(BD1047)和转化生长因子-β1(SB-431542和抗转化生长因子-β1抗体)的抑制剂处理小胶质细胞,可阻断可卡因对艾滋病毒-1表达的刺激。小胶质细胞也结构性地表达Sigma-1受体mRNA。因此,这项研究的结果支持了可卡因的神经免疫药理特性与Sigma-1受体和细胞因子有关的观点。(C)2005年,爱思唯尔出版。
The neuropharmacological properties of cocaine are known to be associated with the activation of sigma-1 receptors. Cocaine also has been shown to alter both cytokine production and HIV-1 expression in mononuclear phagocytes, including microglial cells. This study tested the hypothesis that sigma-l receptors and transforming growth factor (TGF)-beta 1 are involved in cocaine-induced up-regulation of HIV-1 expression in microglial cell cultures. Treatment of microglial cells with cocaine resulted in a concentration-dependent increase in viral expression assessed by measurement of p24 antigen levels in culture supernatants. This cocaine-mediated stimulation of HIV-1 expression was blocked by treatment of microglia with inhibitors of sigma-l receptors (BD1047) and TGF-beta 1 (SB-431542 and anti-TGF-beta 1 antibodies). Microglia were also shown to constitutively express sigma-1 receptor mRNA. Thus, the results of this study support the notion that neuroimmunopharmacological properties of cocaine involve sigma-1 receptors and cytokines. (c) 2005 Published by Elsevier B.V.