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New research challenges long-held beliefs, revealing that sunburn’s acute effects, including inflammation and cell death, are triggered by RNA damage rather than DNA damage. This discovery not only reshapes our understanding of the skin’s defense mechanisms against UV radiation but also paves the way for innovative treatments for sun-related skin conditions.

For years, we’ve been warned about the dangers of the sun: stay out of direct sunlight between noon and 3 p.m., wear sunscreen, and cover up. Yet, despite these precautions, many of us still experience sunburn at some point. The telltale signs—red, painful skin and irritation—are universally recognized.

Traditionally, sunburn has been associated with DNA damage, leading to the well-known effects of inflammation and cell death. However, a groundbreaking study conducted by researchers from the University of Copenhagen and Nanyang Technological University (NTU) in Singapore reveals that RNA, not DNA, is the true instigator of these immediate effects.

“While sunburn does damage DNA, the acute effects of inflammation and cell death actually stem from RNA damage,” explains Assistant Professor Anna Constance Vind from the Department of Cellular and Molecular Medicine, a lead researcher of the study.

The study, published in Molecular Cell, challenges decades of conventional thinking. Researchers discovered that when skin cells are exposed to UV radiation, it is the RNA that takes the brunt of the damage, which in turn triggers the body’s inflammatory response. Unlike DNA, which is more stable and has long-lasting effects, RNA is more transient and typically doesn’t cause permanent mutations. Yet, it plays a crucial role in the skin’s immediate response to UV damage.

RNA’s role in cellular defense has been underappreciated. Messenger RNA (mRNA) serves as a messenger, carrying genetic information from DNA to synthesize proteins. When UV radiation damages mRNA, it sets off a chain of events within cells, including inflammatory signaling and recruitment of immune cells, ultimately leading to sunburn symptoms.

“Damage to mRNA is what initially triggers the skin’s inflammatory response,” says Professor Simon Bekker-Jensen, another lead researcher on the study. “This response, orchestrated by the protein ZAK-alpha, leads to cell death and the visible inflammation associated with sunburn.”

The researchers conducted their study on both mice and human skin cells, observing that the same mechanism was at play in both. By removing the ZAK gene in mice, they were able to prevent the typical inflammatory response, reinforcing the critical role of RNA damage in the skin’s reaction to UV radiation.

This discovery represents a paradigm shift in our understanding of sunburn and the skin’s defense mechanisms. The body’s initial response to UV radiation is faster and more effective than previously thought, driven by RNA damage rather than DNA damage.

“This finding has profound implications for how we approach sunburn prevention and treatment,” says Dr. Franklin Zhong, co-author of the study. “Many inflammatory skin diseases are exacerbated by sun exposure, and understanding the cellular response to UV damage could lead to better treatments for these chronic conditions.”

Ultimately, the research calls for a major revision of our textbooks. What we thought we knew about UV radiation and its effects on the skin is far from the full picture.

“This new knowledge changes everything,” concludes Simon Bekker-Jensen. “We have been conditioned to associate sunburn with DNA damage, but now we need to rethink our understanding and approach. It will influence future research on the effects of UV radiation on the skin.”

Disclaimer: The findings presented in this article are based on a study published in Molecular Cell by researchers from the University of Copenhagen and Nanyang Technological University. Further research is required to explore the full implications of RNA damage in relation to UV exposure and sunburn.

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