A process that alters our genes has been identified as playing a possible role in the development of rheumatoid arthritis. These changes are made by a mechanism called DNA methylation, already known to influence both foetal development and in cancer. Known as epigenetics, this mechanism has now been pinpointed for its part in changing the genes known to affect joint damage and inflammation.
The newest research emerged as part of wider studies into genomics or DNA, which has contributed widely to scientific knowledge of the effects of genetics on rheumatoid arthritis (RA). While certain genetic associations on the development of RA have been identified, scientists know that other factors, including potential epigenetic influences, are also likely to be involved.
Rheumatoid arthritis is an autoimmune disease where the immune system attacks the tissue around the joints. This causes inflammation, leading to painful swelling. It is estimated around 1% of the world’s population has the chronic condition, for which there is no cure.
Our genetics are known to play a significant role in whether we develop autoimmune diseases such as RA. DNA methylation, where a strand of DNA is modified, is a normal part of the process of epigenetic change and crucial to healthy development but may be abnormal in cancers.
The team from the University of California decided to examine the DNA methylation of fibroblast-like synoviocytes (FLS), cells that connect with the immune cells of a patient with RA in a genome-wide evaluation of the process involved in FLS.
The genomic DNA was isolated and evaluated, with the study revealing that FLS present in rheumatoid arthritis has a unique DNA methylome signature, which differentiates it from the FLS present in osteoarthritis and also from normal FLS. The FLS in RA, identified from 28 separate cell lines, was shown to have genes essential for inflammation.
The team concluded that the differentially methylated genes they identified can change the FLS genes and helping in the development of rheumatoid arthritis.
Comments are closed.