A surprising discovery about how skin responds to sun exposure is prompting scientists to rethink their understanding of sunburn. Research published in Molecular Cell reveals that damage to RNA molecules, rather than DNA as long believed, triggers the immediate inflammatory response we know as sunburn.
The international study, conducted by researchers at the University of Copenhagen and Nanyang Technological University in Singapore, demonstrates that a cellular surveillance system monitoring RNA damage serves as the body’s first line of defense against harmful UV radiation.
“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,” says Assistant Professor Anna Constance Vind from the University of Copenhagen’s Department of Cellular and Molecular Medicine, lead author of the study.
A Paradigm Shift in Understanding
While DNA damage from UV exposure remains a serious concern due to its potential long-term effects, the researchers found that RNA damage triggers a more rapid protective response. This quick reaction helps prevent further damage to skin cells through inflammation and controlled cell death.
The researchers identified a protein called ZAK-alpha as the key orchestrator of this protective response. When UV light damages messenger RNA—molecules that carry genetic instructions for making proteins—ZAK-alpha activates a cellular alarm system known as the ribotoxic stress response.
“Everything depends on this one response, which monitors all protein translations occurring,” explains Professor Simon Bekker-Jensen, one of the study’s senior authors. “The cells respond to the RNA damage, realizing that something is wrong, and this is what leads to cell death.”
From Laboratory to Real-World Impact
The research team verified their findings using both mouse models and human skin cells. In experiments with mice lacking the ZAK gene, the typical inflammatory responses to UV exposure disappeared, confirming the protein’s crucial role in the sunburn process.
These findings could lead to new approaches for treating various skin conditions. “Many inflammatory skin diseases are worsened by sun exposure. Understanding how our skin responds at the cellular level to UV damage opens the door to innovative treatments for certain chronic skin conditions,” notes Dr. Franklin Zhong from NTU’s Lee Kong Chian School of Medicine.
Looking Ahead
The discovery challenges decades of established thinking about how skin responds to sun damage. While DNA protection remains important for preventing long-term effects like skin cancer, this new understanding of RNA’s role could lead to better treatments for acute sun damage and related skin conditions.
“This new knowledge turns things upside down,” Bekker-Jensen concludes. “Now we need to rewrite the textbooks, and it will affect future research on the effects of UV radiation on the skin.”