Differential expression of the liver proteome in senescence accelerated mice

Young Moon Cho, Soo Han Bae, Byung Kwon Choi, Sang Yun Cho, Chang Woo Song, Je Kwon Yoo, Young-Ki Paik

Research output: Contribution to journalArticle

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Abstract

The senescence-accelerated mouse (SAM) is a useful animal model to study aging or age-associated disorders due to its inherited aging phenotype. To investigate proteins involved in the aging process in liver, we compared the young (4- or 20-week old) and the aged group (50-week-old) of SAMP8 (short life span) and SAMR1 (control) mice, and identified 85 differentially expressed distinct proteins comprising antioxidation, glucose/amino acid metabolism, signal transduction and cell cycle systems using proteomics tools. For the antioxidation system, the aged SAMP8 mice showed a large increase in glutathione peroxidase and decreases in glutathione-S-transferase and peroxiredoxin, ranging from 2.5- to 5-fold, suggesting lower detoxification potentials for oxidants in the aged SAMP8 liver. Similarly, levels of key glycolytic enzymes decreased greatly in the aged SAMP8 compared to SAMR1, indicating a disturbance in glucose homeostasis that may be closely related to the typical deficits in learning and memory of the aged SAMP8. Protein profiles of amino acid metabolic enzymes suggest that accumulation of glutamine and glutamate in tissues of the aged SAMP8 may be due to hyperexpression of ornithine aminotransferase and/or glutamate dehydrogenase. Decreases in levels of proteins involved in signal transduction/apoptosis (e.g., cathepsin B) in the aged SAMP8 may support the previously proposed negative relationship between apoptosis and aging. However, the changes described above were not markedly seen in the young group of both strains. For cell cycle systems, levels of selenium binding protein increased about four-fold with age in SAMP8. Yet, almost no change occurred in either the young or the aged SAMR1, which may explain problems associated with cell proliferation and tissue regeneration in the aged SAMP8. In conclusion, composite profiles of key proteins involved in age-related processes enable assessment of accelerated senescence and the appearance of senescence-related pathologies in the aged SAMP8.

Original languageEnglish
Pages (from-to)1883-1894
Number of pages12
JournalProteomics
Volume3
Issue number10
DOIs
Publication statusPublished - 2003 Oct 1

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Proteome
Liver
Aging of materials
Signal transduction
Proteins
Selenium-Binding Proteins
Signal Transduction
Cell Cycle
Ornithine-Oxo-Acid Transaminase
Cells
Apoptosis
Peroxiredoxins
Amino Acids
Glucose
Tissue regeneration
Glutamate Dehydrogenase
Cathepsin B
Detoxification
Process Assessment (Health Care)
Cell proliferation

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

Cho, Y. M., Bae, S. H., Choi, B. K., Cho, S. Y., Song, C. W., Yoo, J. K., & Paik, Y-K. (2003). Differential expression of the liver proteome in senescence accelerated mice. Proteomics, 3(10), 1883-1894. https://doi.org/10.1002/pmic.200300562
Cho, Young Moon ; Bae, Soo Han ; Choi, Byung Kwon ; Cho, Sang Yun ; Song, Chang Woo ; Yoo, Je Kwon ; Paik, Young-Ki. / Differential expression of the liver proteome in senescence accelerated mice. In: Proteomics. 2003 ; Vol. 3, No. 10. pp. 1883-1894.
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Cho, YM, Bae, SH, Choi, BK, Cho, SY, Song, CW, Yoo, JK & Paik, Y-K 2003, 'Differential expression of the liver proteome in senescence accelerated mice', Proteomics, vol. 3, no. 10, pp. 1883-1894. https://doi.org/10.1002/pmic.200300562

Differential expression of the liver proteome in senescence accelerated mice. / Cho, Young Moon; Bae, Soo Han; Choi, Byung Kwon; Cho, Sang Yun; Song, Chang Woo; Yoo, Je Kwon; Paik, Young-Ki.

In: Proteomics, Vol. 3, No. 10, 01.10.2003, p. 1883-1894.

Research output: Contribution to journalArticle

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AU - Cho, Young Moon

AU - Bae, Soo Han

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Cho YM, Bae SH, Choi BK, Cho SY, Song CW, Yoo JK et al. Differential expression of the liver proteome in senescence accelerated mice. Proteomics. 2003 Oct 1;3(10):1883-1894. https://doi.org/10.1002/pmic.200300562