The long term goals of the McNulty lab are to develop strategies to prevent osteoarthritis and to promote tissue repair and regeneration following joint injury. In order to achieve these goals, we need to understand the mechanisms necessary for tissue repair and regeneration and how they are altered with aging and joint injury. Specifically, we are working to enhance the integrative repair of meniscus to restore meniscal function and decrease the risk of osteoarthritis development. We have identified IL-1 and TNF as inhibitors of integrative meniscal repair and are developing novel methods to suppress inflammation and the downstream mediators of these cytokines to promote tissue repair. Furthermore, we are working to understand the pathways that are activated by normal and injurious mechanical loading of joint tissues and how these mechanotransduction pathways are altered during aging. A greater understanding of alterations in mechanosensitive signaling mechanisms with aging and injury will likely reveal potential targets to prevent tissue degeneration and osteoarthritis.
Meniscal lesions are common problems in orthopaedic surgery and sports medicine, and injury or loss of the meniscus accelerates the onset of knee osteoarthritis.
Posttraumatic arthritis commonly develops following articular fracture.
Osteoarthritis (OA) is a progressive degenerative disease of articular cartilage and surrounding tissues, and is associated with both advanced age and joint injury.
Collagen II is the major protein component of articular cartilage and forms the collagen fibril network, which provides the tensile strength of cartilage.
The objective of this study was to investigate the expression of the chemokine CXCL10 and its role in joint tissues following articular fracture.
OBJECTIVE: To evaluate the dehydroascorbate (DHA) transport mechanisms in human chondrocytes.
OBJECTIVE: Meniscal tears are a common knee injury and increased levels of interleukin-1 (IL-1) have been measured in injured and degenerated joints.
OBJECTIVE: To examine the hypotheses that increasing concentrations of interleukin-1 (IL-1) or tumor necrosis factor alpha (TNFalpha) inhibit the integrative repair of the knee meniscus in an in vitro model system, and that inhibitors of these cyt
Point mutations in the calcium-permeable TRPV4 ion channel have been identified as the cause of autosomal-dominant human motor neuropathies, arthropathies, and skeletal malformations of varying severity.