PMID- 21286834
OWN - NLM
STAT- MEDLINE
DCOM- 20120229
LR  - 20230602
IS  - 1557-1904 (Electronic)
IS  - 1557-1890 (Print)
IS  - 1557-1890 (Linking)
VI  - 6
IP  - 4
DP  - 2011 Dec
TI  - HIV-1 gp120-induced axonal injury detected by accumulation of beta-amyloid precursor 
      protein in adult rat corpus callosum.
PG  - 650-7
LID - 10.1007/s11481-011-9259-6 [doi]
AB  - HIV-1 brain infection induces neurodegeneration. While most studies focus on 
      HIV-1-mediated neuronal injury, relatively few have investigated HIV-1-associated 
      white matter damage. Corpus callosum (CC) is one of frequently involved white 
      matter structures in HIV-1-associated white matter damage. Utilizing a model of 
      ex vivo treatment of brain slice containing CC with HIV-1 glycoprotein 120 
      (gp120), we examined axonal injury by analyzing beta-amyloid precursor protein 
      (beta-APP) accumulation in the axon. Incubation of CC slice with gp120 produced a 
      significant higher density of beta-APP in the CC tissue compared with 
      non-gp120-treated controls, suggesting the presence of axonal damage in the CC. 
      The gp120-induced CC axonal damage was blocked by a chemokine CXCR4 receptor 
      antagonist T140 but not by an NMDA receptor blocker MK801 as demonstrated by 
      Western blot analysis of beta-APP, indicating that gp120 evokes the CC axonal injury 
      through CXCR4 receptor. Immunocytochemical studies revealed a surprisingly high 
      density of CXCR4-positive immunoreactivity in the CC. The CXCR4-positive labeling 
      was distributed along the nerve fibers. Moreover, double labeling of anti-CXCR4 
      with either anti-neuronal nuclei or anti-myelin/oligodendrocyte-specific protein 
      antibody revealed co-localization of CXCR4 and myelin/oligodendrocytes in some 
      fiber-like structures, inferring that some neurons and oligodendrocytes in the CC 
      express CXCR4. Taken together, these results indicate that gp120 induced axonal 
      damage via CXCR4 in the CC.
FAU - Zhang, Jingdong
AU  - Zhang J
AD  - Department of Pharmacology and Experimental Neuroscience, University of Nebraska 
      Medical Center, Omaha, NE 68198-5880, USA.
FAU - Liu, Jianuo
AU  - Liu J
FAU - Katafiasz, Bryan
AU  - Katafiasz B
FAU - Fox, Howard
AU  - Fox H
FAU - Xiong, Huangui
AU  - Xiong H
LA  - eng
GR  - R56 NS041862-10A1/NS/NINDS NIH HHS/United States
GR  - P30 MH062261/MH/NIMH NIH HHS/United States
GR  - R01 NS041862/NS/NINDS NIH HHS/United States
GR  - R01 NS063878-03/NS/NINDS NIH HHS/United States
GR  - R01 NS 041862/NS/NINDS NIH HHS/United States
GR  - R01 NS063878/NS/NINDS NIH HHS/United States
GR  - R56 NS041862/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20110202
PL  - United States
TA  - J Neuroimmune Pharmacol
JT  - Journal of neuroimmune pharmacology : the official journal of the Society on 
      NeuroImmune Pharmacology
JID - 101256586
RN  - 0 (Amyloid beta-Protein Precursor)
RN  - 0 (HIV Envelope Protein gp120)
RN  - 0 (Receptors, CXCR4)
RN  - 0 (gp120 protein, Human immunodeficiency virus 1)
SB  - IM
MH  - Amyloid beta-Protein Precursor/*metabolism
MH  - Animals
MH  - Axons/metabolism/*pathology/virology
MH  - Blotting, Western
MH  - Corpus Callosum/metabolism/*pathology/virology
MH  - HIV Envelope Protein gp120/*metabolism/pharmacology
MH  - Immunohistochemistry
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, CXCR4/metabolism
PMC - PMC3165079
MID - NIHMS298575
EDAT- 2011/02/03 06:00
MHDA- 2012/03/01 06:00
PMCR- 2012/12/01
CRDT- 2011/02/03 06:00
PHST- 2010/12/06 00:00 [received]
PHST- 2011/01/18 00:00 [accepted]
PHST- 2011/02/03 06:00 [entrez]
PHST- 2011/02/03 06:00 [pubmed]
PHST- 2012/03/01 06:00 [medline]
PHST- 2012/12/01 00:00 [pmc-release]
AID - 10.1007/s11481-011-9259-6 [doi]
PST - ppublish
SO  - J Neuroimmune Pharmacol. 2011 Dec;6(4):650-7. doi: 10.1007/s11481-011-9259-6. 
      Epub 2011 Feb 2.