A fascinating news story in the North County Times, “Cause of sunburn’s painful inflammation discovered by UCSD researchers,” reports on how researchers have discovered that sunburns are caused by an immune response to damaged non-coding RNA molecules:
Sunburn’s red badge of agony is caused by damage to the genetic molecule RNA in skin cells, says a team led by researchers at UC San Diego.
Ultraviolet B light damages a certain kind of RNA that does not make proteins in a cell. This damage leads to the release of inflammatory chemicals called cytokines, according to the researchers’ study, released Sunday. It’s all part of the process of removing damaged cells so they can be replaced with new, healthy ones.
The sunburn response itself is produced by the immune system, which targets damaged cells for destruction.
An article at Science Daily puts it this way:
Using both human skin cells and a mouse model, Gallo, first author Jamie J. Bernard, a post-doctoral researcher, and colleagues found that UVB radiation fractures and tangles elements of non-coding micro-RNA — a special type of RNA inside the cell that does not directly make proteins. Irradiated cells release this altered RNA, provoking healthy, neighboring cells to start a process that results in an inflammatory response intended to remove sun-damaged cells.
Why is this relevant? Some proponents of the “junk” DNA argument, who say the genome is mostly functionless vestigial garbage, claim that even if non-coding DNA is transcribed into RNA, that RNA might still be functionless. While there’s still much that we don’t know about the genome, numerous discoveries have been made finding functions for non-coding RNA. This indicates that just because an RNA isn’t translated into protein, that doesn’t necessarily mean the RNA is non-functional. In this case, it turns out that cells use certain types of non-coding RNA as a signal that they have been damaged by UV radiation, triggering an immune response. The technical paper in Nature Medicine explains in more detail:
Exposure to ultraviolet B (UVB) radiation from the sun can result in sunburn, premature aging and carcinogenesis, but the mechanism responsible for acute inflammation of the skin is not well understood. Here we show that RNA is released from keratinocytes after UVB exposure and that this stimulates production of the inflammatory cytokines tumor necrosis factor ? (TNF-?) and interleukin-6 (IL-6) from nonirradiated keratinocytes and peripheral blood mononuclear cells (PBMCs).
(Jamie J. Bernard, Christopher Cowing-Zitron, Teruaki Nakatsuji, Beda Muehleisen, Jun Muto, Andrew W Borkowski, Laisel Martinez, Eric L Greidinger, Benjamin D Yu, Richard L. Gallo, “Ultraviolet radiation damages self noncoding RNA and is detected by TLR3,” Nature Medicine (July 8, 2012).))
The research paper states: “These findings establish that UVB damage is detected by TLR3 and that self-RNA is a damage-associated molecular pattern that serves as an endogenous signal of solar injury.” This study thus suggests yet another example of non-coding RNA that is important to cellular function.
Image: Friction NYC/Flickr.