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 and sunburn damage
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,” Bekker-Jensen elaborated.
“The cells respond to the RNA
damage, realizing that something is wrong, and this is what leads to cell
death.”
Paradigm shift
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.
Credit: Earth.com
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