A previously unstudied protein in the framework of osteoarthritis may be critical in the prevention of the disease, according to groundbreaking new research published in the journal Science Advances, which included work by Justin Parreno, an assistant professor at the University of Delaware.
Osteoarthritis is an irreversible, painful and debilitating condition of the joints characterized by breakdown of the cartilage that cushions the ends of the bones, called articular cartilage. It occurs most often in the hands, knees or hips and is the most common type of arthritis, affecting more than 32.5 million Americans, according to the Centers for Disease Control and Prevention.
Parreno was a doctoral student at the University of Toronto when he found that the protein called adseverin helps keep the articular cartilage healthy. This is the first time a specific protein associated with cell structure has been identified to be protective against osteoarthritis.
The discovery came almost by accident. He and his colleagues were working on another cartilage therapy when Parreno found that healthy cartilage cells contain large amounts of adseverin while unhealthy cartilage cells do not. The amount of adseverin ultimately regulates the structural scaffolding of cells, called filamentous(F) actin.
F-actin acts like a shield against the stresses on cartilage cells that happen when the joints move. Losing F-actin causes the cells to eventually die.
“The cells are really round, and you have F-actin around the cells,” said Parreno, a member of UD’s Department of Biological Sciences. “If you lose F-actin, those cells are sensitive because there is mechanical stress on them, and they will probably undergo death. Dead cells aren’t able to produce the molecules that are required to regenerate cartilage, and eventually the cartilage degrades.”
Not only do the cells die, but the remaining cells start to produce molecules that cause additional problems in the cartilage.
“The cells that remain are also producing hypertrophic molecules resulting in mineralization and tissue stiffness which leads to a really bad joint,” Parreno said.
Current treatments for osteoarthritis either involve surgery or are aimed at controlling the pain. While Parreno notes the research has not been tested in humans, he said the findings may open doors to therapeutics targeting the protein.
“If we’re able to maintain the levels of adseverin, or alternatively somehow figure out how to keep that F-actin at a high enough level, perhaps we can prevent cell death,” he said. “We’ve got to keep these cells alive and healthy.”
