Proteomic study of neuron and astrocyte cultures from senescence-accelerated mouse SAMP8 reveals degenerative changes.
Senescence-accelerated prone (SAMP) strain 8 mice suffer an earlier development of cognitive age-related pathologies and a shorter life span than conventional mice. Protein alterations in astrocytes, in addition to those in neurons, may contribute to neurodegenerative damage. We applied proteomics techniques to study cell-specific early markers of brain aging-related degeneration in SAMP8. The two-dimensional protein expression patterns of the SAMP8 neuron and astrocyte cultures were compared with those obtained from senescence-accelerated resistant mouse strain 1 cultures. Differentially expressed spots were identified by matrix-assisted laser desorption/ionization-time of flight peptide map fingerprinting and database search. Proteins belonged to cell pathways of energy metabolism, biosynthesis, cell transduction and signaling, stress response, and the maintenance of cytoskeletal functions. Most of the changes were cell type specific. However, there was a general increase in cell transduction, signaling, and stress-related proteins and a decrease in cytoskeletal proteins. In addition, neurons showed an increased expression of proteins involved in biosynthetic pathways. A number of the protein alterations have been previously reported in the brain tissue proteome of SAMP8, aged brain or Alzheimer's disease brain. Alterations in neuron and astrocyte proteoma indicated that both cell types are involved in the brain degenerative changes of SAMP8 mice. However, network analysis suggests that neuronal changes are more complex and have a greater influence.
Díez-Vives
Cristina
C
Department of Brain Ischemia and Neurodegeneration, Institut d'Investigacions Biomèdiques de Barcelona, CSIC-IDIBAPS, Barcelona, Spain.
Gay
Marina
M
García-Matas
Silvia
S
Comellas
Francesc
F
Carrascal
Montserrat
M
Abian
Joaquín
J
Ortega-Aznar
Arantxa
A
Cristòfol
Rosa
R
Sanfeliu
Coral
C
D000375:Aging / Q000235:genetics* / Q000502:physiology; D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000473:pathology; D019295:Computational Biology / Q000379:methods; D004195:Disease Models, Animal; D015180:Electrophoresis, Gel, Two-Dimensional / Q000379:methods; D004622:Embryo, Mammalian; D005786:Gene Expression Regulation / Q000502:physiology; D020271:Heredodegenerative Disorders, Nervous System / Q000378:metabolism* / Q000473:pathology*; D053858:Metabolic Networks and Pathways / Q000235:genetics; D051379:Mice; D008815:Mice, Inbred Strains; D009474:Neurons / Q000378:metabolism*; D010449:Peptide Mapping / Q000379:methods; D040901:Proteomics / Q000379:methods*