 | Mayda Hernandez University of Puerto Rico, Río Piedras ChemistryMentor(s)Scott Goldman, V.M.D. Shengkan (Victor) Jin, Ph.D. Department of Pharmacology UMDNJ-Robert Wood Johnson Medical School |
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| The effect of Beclin 1 heterozygosity on Aging in a mouse model | ||
| The process of macroautophagy has been linked to the process of aging in eukaryotic organisms in multiples studies, but the mechanism behind this relationship has not yet been revealed. In this study, we explored the effect of decreased autophagy via the Beclin1 +/- knock-out mouse model on the physiologic and biochemical aspects of the process of aging with respect to the phenomenon of cellular senescence. Preliminary data revealed an increase in a marker of cellular senescence, p16, in autophagy-deficient Atg5 +/- mouse embryonic fibroblasts (MEF) compared to their wild-type counterparts. Liver tissue was obtained from twenty-four month old male Beclin 1 +/- knock-out and Beclin 1 +/+ wild-type mice and used to generate tissue lysates. Lysates were then subjected to western blot analysis for markers of cellular senescence including the aging-related protein p16. Contrary to the results obtained from MEFs, the results of this analysis showed no significant difference in p16 expression between the mutant and wild-type mice. Physiological data was obtained using the rotarod test to assess the strength and overall fitness of mutant and wild-type mice. The latency to fall from the rod was measured for each mouse over three trials and the results were averaged and statistically analyzed using MS Excel. Initial analysis showed no statistical difference between the knock-out and the wild-type mice groups. Ongoing studies including further rotarod testing of different age and gender mouse groups, vertical rod testing and open field testing are currently underway to provide more data. Further testing is needed to study the effect of autophagy on the process of aging in the Beclin 1 +/- knock-out mouse model. |