AI Article Synopsis
- The study investigates how osmotic stress affects the DNA damage response in the epidermis, particularly focusing on keratinocytes, which make up the outer layer of skin.
- It highlights that osmotic stress influences gene transcription related to both osmotic stress and UV-induced DNA damage, showcasing the complex interaction between different cellular stress responses.
- Researchers found that keratinocytes under osmotic stress showed lower levels of γH2AX, a marker of DNA damage, suggesting that osmotic stress may help modulate the severity of DNA damage caused by UV exposure or oxidative stress.
Article Abstract
The human skin and in particular its outermost layer, the epidermis, protects the body from potentially harmful substances, radiation as well as excessive water loss. However, the interference between the various stress responses of the epidermal keratinocytes, which often occur simultaneously, is largely unknown. The focus of this study was to investigate the interference between osmotic stress and DNA damage response. In addition to revealing the already well-described regulation of diverse gene sets, for example, cellular processes such as transcription, translation, and metabolic pathways (e.g., the KEGG citrate cycle and Reactome G2/M checkpoints), gene expression analysis of osmotically stressed keratinocytes revealed an influence on the transcription of genes also related to UV-induced DNA damage response. A gene network regulating the H2AX phosphorylation was identified to be regulated by osmotic stress. To analyze and test the interference between osmotic stress and DNA damage response, which can be triggered by UV stress on the one hand and oxidative stress on the other, in more detail, primary human keratinocytes were cultured under osmotic stress conditions and subsequently exposed to UV light and HO, respectively. γH2AX measurements revealed lower γH2AX levels in cells previously cultured under osmotic stress conditions.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8946833 | PMC |
| http://dx.doi.org/10.3390/cells11060959 | DOI Listing |
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