Mode of injury and level of synovitis alter inflammatory chondrocyte gene expression and associated pathways.
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2024-11
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Although various joint injuries result in post-traumatic osteoarthritis (PTOA), differences in chondrocyte response to specific injuries, such as blunt compression or fracture, are unclear. Furthermore, the role of underlying joint inflammation, or synovitis, is often not considered. We investigated how injury mechanisms and underlying synovitis affect chondrocyte gene expression using osteochondral injury models with synovial co-culture. We hypothesized that the state of synovitis as well as the mechanism of biomechanical cartilage injury differentially alter the gene expression of chondrocytes and that these responses are regulated by the pro-inflammatory cytokine interleukin 1 (IL-1). The mechanism of injury and level of synovial inflammation both significantly regulated chondrocyte gene expression and associated pathways, uncovering distinct characteristics of fracture and compression injury mechanisms. Targeting IL-1 following injury reduced the inflammatory response and could have clinical implications. The results from this study show that crosstalk between biomechanics and inflammation in the context of synovitis and cartilage injury mechanism is an important consideration for PTOA.
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Libke, Megan L, Daniel J Cunningham, Bridgette D Furman, John S Yi, Jonathan M Brunger, Virginia B Kraus, Farshid Guilak, Amy L McNulty, et al. (2024). Mode of injury and level of synovitis alter inflammatory chondrocyte gene expression and associated pathways. Scientific reports, 14(1). p. 28917. 10.1038/s41598-024-71964-5 Retrieved from https://hdl.handle.net/10161/34847.
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Scholars@Duke
John S Yi
I am an immunologist, with a focus to characterize the immune system in response to infectious and non-infectious diseases including cancer, HIV, autoimmune disease, and transplantation. My goals are to identify novel biomarkers/immune signatures that clinicians can utilize to diagnosis, predict disease outcomes, and determine patients' response to treatment.
Virginia Byers Kraus
Virginia Byers Kraus, MD, PhD, is the Mary Bernheim Distinguished Professor of Medicine, Professor of Orthopaedic Surgery, Professor of Pathology and a faculty member of the Duke Molecular Physiology Institute in the Duke University School of Medicine. She is a practicing Rheumatologist with over 30 years’ experience in translational musculoskeletal research focusing on osteoarthritis, the most common of all arthritides. She trained at Brown University (ScB 1979), Duke University (MD 1982, PhD 1993) and the Duke University School of Medicine (Residency in Internal Medicine and Fellowship in Rheumatology). Her career has focused on elucidating osteoarthritis pathogenesis and translational research into the discovery and validation of biomarkers for early osteoarthritis detection, prediction of progression, monitoring of disease status, and facilitation of therapeutic developments. She is co-PI of the Foundation for NIH Biomarkers Consortium Osteoarthritis project. Trained as a molecular biologist and a Rheumatologist, she endeavors to study disease from bedside to bench.
Amy Lynn McNulty
The McNulty Lab is working to develop strategies to prevent osteoarthritis and to promote tissue repair and regeneration following joint injury. In order to accomplish this, we are working in three main areas. 1) We are working to understand the pathways that are activated by normal and injurious mechanical loading of cartilage and meniscus and how these mechanotransduction pathways are altered during aging, injury, and tissue degeneration. A greater understanding of alterations in mechanosensitive signaling mechanisms with aging and injury will likely reveal potential targets to promote tissue repair and prevent tissue degeneration and osteoarthritis development. 2) We are developing meniscus tissue engineered constructs that will be utilized to repair and replace meniscus tissue lost due to injury and surgical resection. 3) We are focusing on the biological and biomechanical changes that occur in the joint following meniscus injury and how these may contribute to osteoarthritis development.
Steven Arthur Olson
As an Orthopedic Surgeon my primary focus of research is joint preservation. My primary clinical interests are Orthopedic Trauma and Hip Reconstruction.
In Orthopedic Trauma my research interests are 1) Basic science investigations of articular fractures with two current animal models in use. 2) Clinical research includes evaluation of techniques to reduce and stabilize articular fractures, as well as management of open fractures.
In the area of Hip Reconstruction my areas of research are 1) Hip Arthroscopy and treatment of hip disorders, and treatment of labral tears in the treatment of hip pain. 2) Periacetabular osteotomy for the treatment of hip dysplasia.
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