Aging is a complex biological process characterized by a gradual decline in physiological functions and an increased susceptibility to diseases. Cellular senescence is a fundamental mechanism underlying aging, where cells irreversibly stop dividing in response to stress or damage, contributing to tissue dysfunction over time. While senescence has a protective role against tumorigenesis by preventing proliferation of damaged cells, the accumulation of senescent cells and their pro-inflammatory secretions play a significant role in the aging process and the development of age-related diseases.
Key markers such as the senescence-associated β-galactosidase (β-Gal) activity provides a valuable tool for identifying and studying senescent cells. Additionally, p62 (also known as SQSTM1), mainly known to be involved in autophagy, has been recently linked to accelerated aging and age-related pathologies.
We therefore examined these markers in the cortex of SAMP8 mice, a model organism known for its accelerated aging characteristics, compared to senescence resistant control mice (SAMR1).
Here, we thus present quantification of two key biomarkers, β-Gal activity and p62 levels, in the cortex of SAMP8 and SAMR1 mice at the age of 5 and 9 months.
As expected, β-Gal activity is significantly increased in the cortex of SAMP8 mice compared to SAMR1 mice at both ages, indicating increased cellular senescence in SAMP8 mice (Figure 1 A).
Similarly, p62 levels are significantly elevated in SAMP8 mice at both age groups, suggesting additionally altered autophagy processes in these mice compared to SAMR1 already at early age (Figure 1 B).
Figure 1: Senescence and autophagy marker in the cortex of SAMP8 and SAMR1 mice at the age of 5 and 9 months. β-galactosidase (β-Gal) activity (A) as well as p62 protein levels (B) were assessed in cortical samples of 5 and 9 months old SAMP8 and SAMR1 control animals (n=4-8 per group). Two-way ANOVA followed by Bonferroni’s post hoc test. Mean ± SEM. **p <0.01; ***p <0.001.
Understanding these markers and their roles in senescence can lead to significant advancements in aging research and therapeutic development.
Contact us today to get your senescence study in SAMP8 mice started!
