Elevated levels of tissue biomarkers microRNA-181a-5p and microRNA-4454 may cause inflammation, cartilage destruction, and cartilage depletion, contributing to joint degeneration associated with spine osteoarthritis, scientists suggest.
The research team, from the Krembil Research Institute, published their study recently in Journal of Clinical Investigation Insight.
“These biomarkers are actively involved in increasing inflammation and destructive activities in spine cartilage and assist in its destruction,” says principal investigator Mohit Kapoor, PhD, senior scientist at the Krembil Research Institute and associate professor in the Department of Surgery and the Department of Laboratory Medicine and Pathobiology at the University of Toronto, in a media release from University Health Network.
In their study, Kapoor and his team looked at tissue biopsies from 55 patients undergoing decompression or discectomy at the Krembil Neuroscience Centre at Toronto Western Hospital, and explored the role, functioning, and signaling mechanisms of the two tissue biomarkers.
The team screened 2,100 microRNAs and found that measuring the levels of these two specific biomarkers can help clinicians determine the stage to which the disease has progressed, and provide a tool for determining the degree of cartilage destruction, the release notes.
“These are biologically active molecules. By detecting them in the tissue biopsies, we have a tool for determining the stage of spine osteoarthritis,” Kapoor says. “What is really significant, however, is we have discovered that these biomarkers are actively involved in destroying cartilage and increasing inflammation. Furthermore, they promote cartilage cells to die and deplete the most important component of your cartilage, which is your collagen.”
“The most critical aspect of this discovery is that we have found that they are active. Now that we know what they are, we are currently looking at blocking them and restoring the joint,” he adds.
[Source(s): University Health Network, Newswise]
