The hallmark of sunburn – the reddish, painful yet protective immune response from over exposure to ultraviolet (UV) radiation — is a consequence of RNA damage to skin cells, reports a team of UC San Diego School of Medicine researchers and their colleagues.
Using human skin cells and a mouse model, UVB radiation (wavelengths range of 315-280 nanometers) was shown to fracture and tangle 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, triggering an inflammatory response by healthy, neighboring cells intended to remove sun-damaged cells.
Understanding the newly discovered pathway might lead to ways of blocking the process, not only in sunburn sufferers but in patients with diseases, like psoriasis, that are treated by UV light but at an increased risk of skin cancer.
The findings are reported in Nature Medicine. News release at
Key step identified in immune system-fueled inflammation
Neutrophils are the body’s first line of defense against bacterial infections. Like other immune cells, neutrophils travel throughout the body via the blood stream to sites of infection, injury, or inflammation. However, the increased blood flow that often accompanies inflammation could whisk these cells past their intended target.
Researchers at the La Jolla Institute for Allergy & Immunology report the discovery of neutrophils using sling-like membrane tethers to adhere to blood vessel walls during periods of increased blood flow. By separating their cytoskeleton from the cellular membrane, neurophils wrap the sling around themselves, secure a hold, then migrate through blood vessel walls to accomplish their infection-fighting work.
The study appears in the journal Nature. News release at
Treating diabetes via the biological clock investigated
UC San Diego biologists have discovered a chemical that offers a completely new direction for drug development to treat metabolic disorders such as type 2 diabetes. The discovery came as a surprise because the isolated chemical does not directly control glucose production in the liver. Instead, the chemical affects the activity of a key protein that regulates the internal mechanisms of our daily night and day activities — the so-called biological clock.
To maintain a steady supply of glucose in our bloodstream, hormones signal we’re in a fasting state while we sleep and stimulate the liver to produce needed glucose. While we’re active our biological clock shuts down fasting signals because glucose is derived from the food we eat.
Scientists had long suspected that diabetes and obesity could be linked to problems in the biological clock. For example, altering the biological clock that controls fasting signals in lab mice often leads to obesity and diabetes. Two years ago, UCSD researchers discovered the first biochemical link between the biological clock and diabetes: a protein known as cryptochrome that regulates both the biological clock and glucose production in the liver.
Now, the same team has discovered a small molecule — one that can be easily developed into a drug — that controls the timekeeping mechanisms of cryptochrome in such a manner that it can repress liver production of glucose.
The finding is published in the journal Science. News release at