ANP32A, a protein involved in multiple cellular processes, protects cartilage in the joints against degradation by damaging oxidation, preventing the development and progression of osteoarthritis, a recent study suggests.
The study, conducted by Frederique Cornelis and colleagues, was published recently in Science Translational Medicine.
Their findings suggest that some antioxidant treatments could be useful in preventing further cartilage damage and reducing the severity of osteoarthritis, and potentially other bone and brain disorders, according to a media release from the American Association for the Advancement of Science.
The researchers note that ANP32A levels are decreased in osteoarthritis tissue samples from humans and mice, leading them to ask what function the protein might play in normal tissues. Gene expression profiling revealed that ANP32A increases the levels of an enzyme called ATM as part of the response against oxidative stress in joint cartilage cells. Interestingly, doses of the antioxidant N-acetyl-cysteine (NAC) in drinking water reduced osteoarthritis symptoms and cartilage damage in mice deficient in ANP32A.
The researchers also discovered that ANP32A deficiency was linked to osteopenia (bone loss) and a neurological disease similar to ataxia-telangiectasia (A-T) in mice, and that these disorders could also be treated with NAC antioxidant therapy, the release explains.
[Source(s): American Association for the Advancement of Science, EurekAlert]