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Changes in neuronal protein expression in LP-BM5-infected mice
Kanako Takahashi1, Kuniaki Saito, Junichi Masuda
1Department of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Japan.
Abstract:
Murine acquired immunodeficiency syndrome (MAIDS) induced by LP-BM5 murine leukemia virus is used as a model of human immunodeficiency virus (HIV)-related neurologic dysfunction. Mice infected with LP-BM5 have mnemonic abnormalities (i.e., spontaneous alternation behavior in the Y-maze and performance in the Morris water maze) and biochemical alternations (i.e., cytokines, platelet-activating factor, quinolinate, glutamate and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor) that produce neurologic symptoms similar to those observed in HIV-related neurologic dysfunction. To identify proteins associated with dysmnesia in the MAIDS model, we examined the expression of neuronal proteins in LP-BM5-infected mice using two-dimensional polyacrylamide gel electrophoresis (2-DE). Neuronal protein expression in LP-BM5-infected mice was compared with that in non-infected mice using the Image Master 2D. We detected approximately 800 protein spots, of which 35 were distinguishable between non-infected and LP-BM5-infected mice. Most of these spots were downregulated in LP-BM5-infected mice. Three of the spots were identified as 14-3-3 protein zeta/delta, synapsin 2 and protein disulfide isomerase using a capillary nanoliquid chromatography tandem mass spectrometric system. We verified the expression levels of these proteins by Western blot. Analysis of these 35 spots could provide insight into mechanisms of dysmnesia in the MAIDS model of HIV-related neuronal dysfunction.
Insights
Murine acquired immunodeficiency syndrome (MAIDS) models human immunodeficiency virus (HIV) neurological issues. Researchers identified key neuronal proteins, like 14-3-3 zeta/delta, downregulated in MAIDS mice, offering insights into memory loss mechanisms.
Area of Science:
- Neuroscience
- Immunology
- Virology
Background:
- Murine acquired immunodeficiency syndrome (MAIDS) serves as a model for human immunodeficiency virus (HIV)-related neurological dysfunction.
- LP-BM5 virus infection in mice causes mnemonic and biochemical abnormalities mirroring HIV-related neurological symptoms.
Purpose of the Study:
- To identify specific neuronal proteins associated with memory impairment (dysmnesia) in the MAIDS model.
- To understand the molecular mechanisms underlying neurological dysfunction in MAIDS.
Main Methods:
- Two-dimensional polyacrylamide gel electrophoresis (2-DE) was employed to analyze neuronal protein expression in LP-BM5 infected mice compared to controls.
- Image Master 2D software was used for quantitative analysis of protein spots.
- Capillary nanoliquid chromatography tandem mass spectrometry and Western blot were utilized for protein identification and verification.
Main Results:
- Approximately 800 protein spots were detected, with 35 showing significant differences between infected and non-infected mice.
- The majority of differentially expressed proteins were downregulated in LP-BM5 infected mice.
- Three proteins were identified: 14-3-3 protein zeta/delta, synapsin 2, and protein disulfide isomerase.
Conclusions:
- The study identified specific downregulated neuronal proteins in the MAIDS model, contributing to the understanding of HIV-related neurological dysfunction.
- These findings provide potential molecular targets for further investigation into the mechanisms of dysmnesia in MAIDS.
- The identified proteins may play crucial roles in the pathogenesis of memory deficits observed in this model.
