Spending enough time in the sun without proper protection can leave us looking and probably feeling like a lobster ready for the plate.
THE conventional explanation For the painful skin inflammation response, involves a cascade of effects triggered by breaks in the tissue’s DNA.
It now appears that we might have had this key detail incorrect all along. According to a new study involving mice and human skin cells, the first moments of sunburn are a little different than everyone expected.
“Sunburn damages DNA, leading to cell death and inflammation. So the textbooks say, ” said Anna Constance Vind, a molecular biologist at the University of Copenhagen who led an investigation that challenges what we thought we knew about sun damage.
“But in this study, we were surprised to learn that it is the result of RNA damage, not DNA damage, that causes the acute effects of sunburn.”
The term sunburn is something of a misnomer. Unlike low-level thermal burns, which result from heat making a mess of your body’s proteins, burn damage is caused by prolonged doses of shorter type “B” ultraviolet radiation.
Regardless of how the damage is caused, the result is the same: a variety of cellular stresses alert the immune system to a threat, triggering a domino effect of chemical sirens that widen some blood vessels, constrict others, and increase blood pressure. sensitivity to pain.
Pinning down precisely what these triggers are can be messy. Heat itself can induce responses, for example. Sudden changes in water, reactive oxygen species released from broken compounds, and simple fractures in the cells themselves can all send signals to the immune system that it needs to act quickly.
Because the bonds between nucleic bases can absorb Ultraviolet B photons to the point of breaking and reconfiguring, it has long been assumed that DNA damagein association with other forms of cellular damage, is essential at these early moments of signaling.
“DNA damage is serious because mutations will be passed on to progenitors of cells, RNA damage occurs all the time and does not cause permanent mutations.” said Vind.
“Therefore, we used to believe that RNA is less important, as long as DNA is intact. But in fact, RNA damage is the first to trigger a response to UV radiation.”
Vind and his colleagues demonstrated this using mice genetically engineered to lack a stress response protein called Zak-alphawhich by linking with cellular machines that translate messenger RNA chains into proteins can ring alarm bells when the translation process is not going as planned.
Dosing mice with and without zak-alpha with ultraviolet B or an antibiotic that also triggers the protein in response reveals that the RNA-mediated stress response is essential for creating Sunburn symptoms.
With a series of laboratory experiments on human skin cells designed to test the consequences of UV-induced DNA damage, the team showed significant changes in a cell’s messenger RNA a caused the cell to shut down and the immune system to respond.
Without Zak-alpha, mice exposed to ultraviolet B radiation were not burned like normal, suggesting that RNA damage may also be critical to our body’s sensitivity to sunlight.
Although damage to the core DNA library may be a greater concern, monitoring the cell’s messenger system may give cells the advantage in a more rapid response to the radiation threat.
“The fact that DNA doesn’t control the skin’s initial response to UV radiation, but something else does, and it does it more efficiently and more quickly, is quite the game-changer. paradigm,” said Vind.
By continuing to explore the consequences of RNA damage and its role in stress responses, we may find ways to better treat sunburn and Other Conditions Exacerbated by Sunlight.
This research was published in Molecular cell.