Substance P enhances HIV-1 infection in human fetal brain cell cultures expressing full-length neurokinin-1 receptor

被引:5
|
作者
Schwartz, Lynnae [1 ]
Spitsin, Sergei V. [1 ,2 ]
Meshki, John [1 ,2 ]
Tuluc, Florin [1 ,2 ]
Douglas, Steven D. [1 ,2 ]
Wolfe, John H. [1 ,2 ,3 ]
机构
[1] Childrens Hosp Philadelphia, Res Inst, Philadelphia, PA 19104 USA
[2] Univ Penn, Perelman Sch Med, Dept Pediat, Philadelphia, PA 19104 USA
[3] Univ Penn, Sch Vet Med, WF Goodman Ctr Comparat Med Genet, Philadelphia, PA 19104 USA
关键词
Substance P; Human fetal brain cells; Neurokinin-1; receptor; HIV-1; Aprepitant; VIRUS TYPE-1 INFECTION; PROGENITOR CELLS; ANTAGONIST APREPITANT; CHEMOKINE RECEPTORS; ASTROCYTES; ACTIVATION; MATURATION; MICROGLIA; SYSTEM; NESTIN;
D O I
10.1007/s13365-013-0166-x
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The associations between the neurokinin-1 receptor (NK-1R), substance P (SP), and HIV-1 were investigated in neurosphere-derived cultures of microglial-depleted human fetal brain cells (HFBC). Full-length NK-1R was identified in HFBC cultures. SP treatment of the HFBC increased intracellular calcium mobilization and decreased electrical impedance, both of which were blocked by the NK-1R antagonist aprepitant. SP treatment of HIV-1-infected HFBC upregulated HIV-1 expression. These data show that human neural cells grown from neurospheres express functional full length NK-1R that is responsive to SP, and that SP enhanced HIV-1 infection in HBFC.
引用
收藏
页码:219 / 227
页数:9
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