Main cause of sunburn is finally identified, and it's time to rewrite the textbooks

Sunburn is painful skin damage that we’ve all experienced after spending a bit too much time outdoors without protection from UV rays. Whether it’s from a lazy beach day or an exhilarating hike, the aftermath tells a singular tale – crimson skin and a nagging sting.

We’ve long believed that stepping out into the sun requires ample sunscreen slathering, shade-seeking, and hat-wearing, especially between the peak hours of 12 noon and 3 p.m.

However, researchers at the University of Copenhagen and Nanyang Technological University (NTU Singapore) have made surprising new strides in our understanding of sunburn.

As it turns out, the DNA damage we’ve always associated with sunburn might not be the complete story.

DNA, RNA, and sunburn damage

When it comes to sunburn, the prevailing wisdom suggests that DNA damage triggers inflammation and subsequent cell death.

However, this recent research suggests that the real offender might be RNA, not DNA.

“Sunburn damages the DNA, leading to cell death and inflammation. So the textbooks say,” stated assistant professor Anna Constance Vind from the Department of Cellular and Molecular Medicine at the University of Copenhagen.

“But in this study we were surprised to learn that this is a result of damage to the RNA, not the DNA that causes the acute effects of sunburn.”

But what’s the difference between DNA and RNA? While they share similarities, the two aren’t interchangeable.

DNA is a more consistent molecule, whereas RNA is more transitory.

A particular type of RNA, messenger RNA (mRNA), carries information from DNA to create proteins – the fundamental building blocks of cells.

Importance of RNA

The importance of mRNA in our body’s response to UV radiation can’t be understated.

“DNA damage is serious as the mutations will get passed down to progenies of the cells, RNA damage happens all the time and does not cause permanent mutations,” Vind explained.

“Therefore, we used to believe that the RNA is less important, as long as the DNA is intact. But in fact, damages to the RNA are the first to trigger a response to UV radiation.”

Investigating more deeply into the matter was no small task.

The researchers embarked on a study involving both mice and human skin cells to better understand the consequences of UV radiation on the skin. They discovered a consistent response in both species.

ZAK-alpha – the protector

RNA damage activates a response in ribosomes (protein complexes that interpret the mRNA to assemble proteins).

This process is managed by a protein known as ZAK-alpha, which triggers what is referred to as the “ribotoxic stress response.”

Think of it like a vigilant watchman, always on the lookout for RNA damage. When it detects any, it won’t hesitate to call for backup.

“We found that the first thing the cells respond to after being exposed to UV radiation is damage to the RNA, and that this is what triggers cell death and inflammation of the skin,” explained Professor Simon Bekker-Jensen, who was also from the Department of Cellular and Molecular Medicine.

In mice exposed to UV radiation we found responses such as inflammation and cell death, but when we removed the ZAK gene, these responses disappeared, which means that ZAK plays a key role in the skin’s response to UV-induced damage.

“So you could say that everything depends on this one response, which monitors all protein translations occurring. The cells respond to the RNA damage, realizing that something is wrong, and this is what leads to cell death,” Bekker-Jensen elaborated.

Rethinking sunburn and UV damage

The study’s findings question our long-held beliefs about sunburn and how our skin safeguards itself. It suggests that RNA damage sparks a quicker, more efficient response, which safeguards the skin from additional harm.

“The fact that the DNA does not control the skin’s initial response to UV radiation, but that something else does and that it does so more effectively and more quickly, is quite the paradigm shift,” reflected Vind.

Knowing how our skin reacts to UV damage at a cellular level could potentially transform prevention and treatment approaches to sunburn and other inflammatory skin conditions.

“Many inflammatory skin diseases are worsened by sun exposure. Thus, understanding how our skin responds at the cellular level to UV damage opens the door to innovative treatments for certain chronic skin conditions,” explained Dr. Franklin Zhong, Nanyang assistant professor at NTU’s Lee Kong Chian School of Medicine and a co-author of the study.

Rewriting the textbooks

In closing, it seems now is the time to revise our textbooks and rethink how we perceive the effects of UV radiation on our skin.

“This new knowledge turns things upside down. I think most people associate sunburn with DNA damage; it is established knowledge,” Professor Simon Bekker-Jensen concluded. “But now we need to rewrite the textbooks, and it will affect future research on the effects of UV radiation on the skin.”

The full study was published in the journal Molecular Cell.

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