Objectives: The objectives of these studies was to investigate and model the formation of senescence cells in skin after to environmental insult and to determine if this has a correlation to skin aging.
Introduction: The proliferative cells of the body have been shown to have a limited cell division capacity and eventually stop dividing in a process called cellular senescence. Senescence is characterized by several changes such as enlargement, beta-galactosidase staining and expression of several protein markers such as p16INK4a and the loss of cell division. Senescence has also been shown to be initiated by cellular stresses such as oxidative stress, Grow Factor and DNA damage. The in vivo accumulation of senescent cells has been suggested to be a major causal mechanism of the aging phenotype.
Materials / method: We investigated the effects of pollution and IR on the formation of senescence cells in skin models. Senescence was measured by histological markers such as beta Gal, p16, p21 and Ki67 staining. In addition, SASP markers were assessed by measuring the levels of IL-1, IL-6, IL-8 released into the media.
Results: We have observed increase senescence with the exposure to hydrogen peroxide, UV, pm 2.5 and IR. A significant enhancement of expression in proteins associated with the senescence secretome, IL-1, IL-6, IL-8, VEGF-A, MMP-1, was observed with all of these environmental triggers. These damaging agents trigger the expression of SASP and can be inhibited by use of several agents.
Conclusion: Taken together, this research suggests that preventing the accumulation of senescent cells, or clearing them once formed, is a promising strategy to delay, prevent, or potentially reverse some signs and symptoms of aging.
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