June 10, 2012 § Leave a comment
This is the sort of weather in which I can easily burn within the space of 30 to 45 minutes. That’s assuming I’m fool enough to stand outside in midday with neither sunscreen nor embarrassingly floppy hat. I do actually try to avoid that sort of behavior, but it can happen.
Within the first few hours of such exposure, my skin cells—keratinocytes—will begin churning out everything from inflammatory chemicals to immunosuppressants to nitric oxide, leaving me at once in pain, vulnerable to infection, and hot to the touch. White blood cells and prostaglandins will course through the area, adding to the mess. Worse yet, in some of my skin cells, the UV radiation will physically wrench apart and badly rebind key segments of my DNA, leaving misshapen bulges in its wake—like a long piece of string pinched in spots into tiny, doubled-up loops. My genetic copyediting team might be able to salvage some of these cells but others, past the point of no return, will push their self-destruct button and initiate suicide.
For the next few days, I will spend too much time taking cool showers and feeling sorry for myself.
But there’s one piece to this chain of events that’s missing: how did my skin know in the first place to do all this? What’s the molecular tripwire here?
Enter a new study from a crew of researchers out of San Diego, Miami, and New Jersey. With that question in mind, they performed an elegant series of experiments in both mice and skin cells in a dish. Their answer: it comes down to RNA. Specifically, sun-damaged RNA that tips off a molecular pattern-recognizer, which jumpstarts the inflammatory pathways, which snowballs into a miserable, sunburned chemical party on my skin. « Read the rest of this entry »