The skin serves as our body’s first line of defense against external threats. As we age, however, the epidermis – the outermost layer of skin – gradually becomes thinner and loses its protective strength. Research has long emphasized the benefits of vitamin C (VC) in maintaining skin health and promoting antioxidant properties.

Recently, a team of researchers in Japan made an exciting discovery: VC helps thicken the skin by directly activating genes that control skin cell growth and development. Their findings, published online in the Journal of Investigative Dermatology, suggest that VC may restore skin function by reactivating genes essential for epidermal renewal.

Led by Dr. Akihito Ishigami, Vice President of the Division of Biology and Medical Sciences at Tokyo Metropolitan Institute for Geriatrics and Gerontology, the study used human epidermal equivalents – laboratory-grown models that closely mimic real human skin. In this model, skin cells are exposed to air on the surface while being nourished from underneath by a liquid nutrient medium.

The researchers applied VC at concentrations comparable to those typically transported from the bloodstream into the epidermis and found that VC-treated skin showed a thicker epidermal cell layer without significantly affecting the stratum corneum (the outer layer composed of dead cells) on day seven. By day 14, the inner layer was even thicker, and the outer layer was found to be thinner, suggesting that VC promotes the formation and division of keratinocytes.

Importantly, the study revealed that VC helps skin cells grow by reactivating genes associated with cell proliferation. This process occurs through DNA demethylation – a process in which methyl groups are removed from DNA, allowing for gene expression and promoting cell growth.

The researchers further identified over 10,138 hypomethylated differentially methylated regions in VC-treated skin and observed a 1.6- to 75.2-fold increase in the expression of 12 key proliferation-related genes. When a TET enzyme inhibitor was applied, these effects were reversed, confirming that VC functions through TET-mediated DNA demethylation.

These findings reveal how VC promotes skin renewal by triggering genetic pathways involved in growth and repair. This suggests that VC may be particularly helpful for older adults or those with damaged or thinning skin, boosting the skin’s natural capacity to regenerate and strengthen itself.

“We found that VC helps thicken the skin by encouraging keratinocyte proliferation through DNA demethylation, making it a promising treatment for thinning skin, especially in older adults,” concludes Dr. Ishigami.

This study was supported by grants from the Japan Society for the Promotion of Science (JSPS) KAKENHI: grant number 19K05902.

Cohesin, a protein complex that forms loops in the human genome, plays a crucial role in determining the architecture of our genetic material and regulating gene expression. However, its function and behavior have remained somewhat mysterious until now.

Researcher Professor Eva Estébanez-Perpiñá from the University of Barcelona, along with her team and international collaborators, has made significant strides in understanding how cohesin works. Their study, published in Nucleic Acids Research, sheds light on the protein’s interaction with chromatin structure and its role in altering gene expression.

Cohesin consists of four subunits: SMC1, SMC3, SCC1/RAD21, and STAG (also known as SA or SCC2). Previous studies had identified 25 proteins that regulate these subunits and their biological function. Estébanez-Perpiñá’s team has now discovered how the NIPBL protein interacts with both MAU2 and the glucocorticoid receptor (GR), a transcription factor essential for cellular functions.

This ternary complex, comprising NIPBL, MAU2, and GR, modulates transcription by facilitating the interaction of GR with these two proteins. When GR interacts with NIPBL and MAU2, it alters chromatin structure and affects gene expression. This discovery has significant implications for understanding Cornelia de Lange syndrome, a rare disease caused by mutations in genes involved in cohesin formation.

The researchers used advanced microscopic techniques to visualize real-time molecular complexes binding to chromatin, as well as biochemical and biophysical methods to analyze the complex from different structural and cellular perspectives.

Their findings not only improve our comprehension of cohesin’s role but also highlight its potential involvement in other diseases, such as asthma and autoimmune pathologies. As research continues, scientists will likely uncover more about this enigmatic protein and its intricate relationships with chromatin structure and gene expression.

The article you provided raises critical concerns about the potential consequences of early teenage obesity on future generations. A recent study published in Communications Biology has shed light on the biological mechanism behind this issue, revealing that boys who become overweight in their early teens may pass on harmful epigenetic traits to their children.

Researchers from the University of Southampton and the University of Bergen in Norway investigated the epigenetic profiles of 339 people, aged 7 to 51. They found that fathers who gained weight during adolescence were more likely to have epigenetic changes in over 2,000 sites in 1,962 genes linked with adipogenesis (formation of fat cells) and lipid metabolism in their children.

These epigenetic changes can regulate gene expression and are associated with asthma, obesity, and low lung function. The study found that the effect was more pronounced in female children than male children, with different genes involved.

The findings have significant implications for public health and may be a game-changer in public health intervention strategies. As Professor Cecilie Svanes from the University of Bergen noted, “A failure to address obesity in young teenagers today could damage the health of future generations, further entrenching health inequalities for decades to come.”

The research was funded by the Norwegian Research Council and highlights the importance of addressing childhood obesity globally. As Prof John Holloway from the University of Southampton and the National Institute for Health and Care Research (NIHR) Southampton Biomedical Research Centre added, “Childhood obesity is increasing globally, and the results of this study demonstrate that this is a concern not only for the health of the population now but also for generations to come.”