Audrey McAlinden, Ph.D
Department of Orthopaedic Surgery, Department of Cell Biology & Physiology, Washington University
BJC - Institute of Health
11th floor - RM 11612
Phone: (314) 454-8860
Stemming from our wide-ranging interests in skeletal biology, research in the McAlinden Lab focuses on cartilage tissue, both articular and growth plate cartilage. We aim to better understand how cartilage tissue develops, how it is maintained throughout life, what happens when it breaks down, how to slow down or stop degeneration as well as devise strategies to repair or regenerate cartilage.
Articular cartilage provides our synovial joints with critical load bearing and lubricating function. With respect to the knee and hip joint, this tissue permits us to walk, run marathons or perform other high/low impact athletic activities over and over again in a pain-free setting. However, trauma to the joint can result in malalignment (e.g. due to meniscal or ligament injury) or direct injury to the cartilage resulting in lesions that can progress over time to cause osteoarthritis (OA). OA is a serious and debilitating orthopaedic condition affecting a high percentage of the ageing population, but is also problematic among younger people because of higher incidences of joint trauma as a result of sports injuries as well as obesity. Treatment strategies for end-stage OA, where most of the articular cartilage has been eroded, involve knee replacement surgery. However, post-traumatic osteoarthritis (PTOA) is amenable to other treatment strategies to attempt to prevent progression to end-stage OA.
With this clinical problem in mind, we are addressing important basic science questions with the hope that the knowledge gained from our research could be important in advancing the field of cartilage regenerative medicine as well as identifying new therapeutic targets to ameliorate or halt cartilage breakdown.
Toward this end, we are utilizing a range of molecular, cellular and biochemical techniques, as well as animal models, to determine: 1) intracellular factors (specifically, non-coding microRNAs) that function in regulating mesenchymal stem cell (MSC) differentiation toward the chondrocyte lineage as well as in maintaining homeostasis of differentiated chondrocytes; 2) the effects of an embryonic collagen-derived extracellular matrix on the tissue maintenance, degradation and repair; and 3) the effects of biomaterials on MSC differentiation.
For more information on each of these areas of research, see the Projects link.