Finding Aging-Related Expression Changes in Proteins in Skin Tissue

A great deal of time and effort goes into identifying proteins that are expressed to different degrees in young versus old tissues. It is comparatively easy to find such proteins, the question is always what to do with that information. That levels of a given protein change with age is no guarantee that it is meaningfully involved in aging, or that its role is well known, or even that a good catalog of the other protein machinery that it interacts with will help in the production of interventions to treat aging. Exploration of aging at the level of protein expression is, in large part, quite disconnected from understanding of the causes of aging, or of the consequences of aging. This is the challenge of dealing with an enormously complex biological system: a great deal of work is yet needed to be able to robustly connect what is known of causes, proteomics, and outcomes in aging.

Aging is characterized by the gradual loss of physiological integrity, resulting in impaired function and greater mortality. It is very important to find biomarkers that can prevent aging. In this study, key senescence-related molecules (SRMs) were identified in young and senescent fibroblasts by integrating transcriptome and proteomics from aging tissue/cells, and the correlation between these differentially expressed genes and well-known aging-related pathways. We first combined proteomics and transcriptomics to identify four SRMs. Existing data sets and qPCR confirmed that ETF1, PLBD2, ASAH1, and MOXD1 were identified as SRMs. Then the correlation between SRMs and aging-related pathways was excavated and verified. Next, we verified the expression of SRMs at the tissue level and qPCR, and explored the correlation between them and immune infiltrating cells. Finally, at the single-cell transcriptome level, we verified their expression and explored the possible pathway by which they lead to aging.

Briefly, ETF1 may affect the changes of inflammatory factors such as IL-17, IL-6, and NFKB1 by indirectly regulating the enrichment and differentiation of immune cells. MOXD1 may regulate senescence by affecting the WNT pathway and changing the cell cycle. ASAH1 may affect development and regulate the phenotype of aging by affecting cell cycle-related genes. In conclusion, based on the analysis of proteomics and transcriptome, we identified four SRMs that may affect aging and speculated their possible mechanisms, which provides a new target for preventing aging, especially skin aging.


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