Proteomic study of neuron and astrocyte cultures from senescence accelerated mouse SAMP8
نویسندگان
چکیده
Senescente-accelerated prone (SAMP) strain 8 mice suffer an earlier development of cognitive aging-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 used proteomics to study cell-specific early markers of brain aging-related degeneration in SAMP8. The 2-D protein expression patterns of SAMP8 neuron and astrocyte cultures were compared to those obtained from the senescence-resistant strain 1 (SAMR1) cultures. Differentially expressed proteins identified by MALDI–TOF MS in both cell types belonged to cell pathways of energy metabolism, biosynthesis, cell transduction and signaling, stress response and the maintenance of the cytoskeletal functions. Most changes detected were cell type specific, but there was a general trend of increase of cell transduction, signaling and stress-related proteins and decrease of cytokeletal proteins. Also, neurons showed an increase of the expression of several proteins involved in biosynthetic pathways. As a whole, the alterations of their proteoma indicated that both cell types are involved in the brain degenerative changes of SAMP8 mice, but network analysis suggests that neuronal changes are more complex and influencing. Cell culture proteomics is a powerful tool to discern cell specific changes and contributions to aging-related neuropathologies.
منابع مشابه
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 ...
متن کاملMini review The senescence-accelerated prone mouse (SAMP8): A model of age-related cognitive decline with relevance to alterations of the gene expression and protein abnormalities in Alzheimer’s disease
The senescence-accelerated mouse (SAM) is an accelerated aging model that was established through phenotypic selection from a common genetic pool of AKR/J strain of mice. The SAM model was established in 1981, including nine major senescence-accelerated mouse prone (SAMP) substrains and three major senescence-accelerated mouse resistant (SAMR) substrains, each of which exhibits characteristic d...
متن کاملSingle nucleotide variants (SNVs) define senescence-accelerated SAMP8 mice, a model of a geriatric condition.
One of the major challenges in neurodegenerative research is modeling systemic aging. Here, senescence-accelerated mice such as the multigenic SAMP8 (senescence accelerated prone 8) mice are useful as they are characterized by an early manifestation of senescence that includes a shortened lifespan and impaired brain and immune functions. While SAMP8 mice are widely used tools to address aging a...
متن کاملAge-related changes in the spontaneous motor rhythms of the senescence-accelerated mouse (SAMP8).
The present study examined the effect of age on the spontaneous motor rhythms of mice during wheel running. The spontaneous motor tempo (SMT) of wheel running was measured for the P8 strain of the senescence-accelerated mouse (SAMP8) by recording the sequence of time intervals (measured in milliseconds) for successive revolutions ofa run-wheel over the course of 16 days. Analyses of the distrib...
متن کاملData on the optimization of behavioral tasks for senescence-accelerated mouse prone 8 (SAMP8)
This data article contains the supporting information for the research article entitled "Early onset of behavioral alterations in senescence-accelerated mouse prone 8 (SAMP8)" [1]. Senescence-accelerated mouse prone 8 (SAMP8), which originally developed from AKR/J mice, shows learning and memory impairments at the age of 8-12 months. However, little information is still available on phenotypica...
متن کامل