https://www.newsweekjapan.jp/stories/lifestyle/2025/02/538659_1.php
https://www.newsweekjapan.jp/stories/lifestyle/2025/02/538659_1.php
A protein that switches between cellular “youth” and “aging” may hold the key to reversing cellular aging...
A research team from Osaka University investigated the expression of the protein “AP2A1 (adaptor protein 2 alpha 1 subunit)” in cells of different ages. As a result, they obtained some surprising findings. “When AP2A1 was suppressed in aged cells, aging was reversed and cell rejuvenation was promoted. On the other hand, when AP2A1 was overexpressed in young cells, aging progressed,” they explain.
As we age, cells with reduced activity accumulate in various organs. These “senescent cells” are clearly larger than young cells, and the structure of their “stress fibers”, which are parts of the cell that help with interactions, is also different.
“We still don't fully understand why senescent cells are able to maintain such a large size,” says another author of the study, Pirawan Chantachotikul.
The research team focused on the AP2A1 protein, which is known to produce a large number of stress fibers in senescent cells.
In their research, the team cultured fibroblasts (cells that maintain the structure of tissues) and epithelial cells (cells that cover the inside and outside of skin and organs), and suppressed the production of AP2A1 in senescent cells while increasing its expression in young cells, and analyzed the effects of this.
In addition, it was found that AP2A1 is closely related to another protein called “integrin beta 1”. This protein helps cells adhere to the surrounding collagen. The research team explains that these two proteins move along stress fibers within the cell.
Furthermore, integrin beta 1 may strengthen cell-substrate (CS) adhesion in fibroblasts and be involved in the formation of enlarged stress fibers seen in senescent cells.
Based on the relationship between AP2A1 and senescent cells, there is the possibility that this protein could be used as a “cell senescence marker”, and it is also hoped that the findings of this research could lead to new treatments for age-related diseases in the future.
[References]
Chantachotikul, P., Liu, S., Furukawa, K., & Deguchi, S. (2025). AP2A1 modulates cell states between senescence and rejuvenation. Cellular Signalling, 127.
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