Assistant Research Professor in Cell Biology
Member of Duke Molecular Physiology Institute
Senior Fellow in the Center for the Study of Aging
Member of the Duke Cancer Institute
Affiliate of the Duke Regeneration Center
Jim White is Assistant Professor in Medicine, Division of Hematology and Senior Fellow in the Duke Center for Aging and Human Development. He earned a PhD in Exercise Science, specializing in skeletal muscle biology, at the University of South Carolina, Columbia, followed by a postdoctoral fellowship in the lab of Bruce Spiegelman at Harvard Medical School. There he worked in the areas of muscle metabolism and metabolic disease. His laboratory studies mechanisms of age-related functional decline of stem cells within skeletal muscle, vasculature and the immune system. His research program employs a wide range of investigation including in vitro cellular assays, mouse models and human studies. The overarching goal of this work is to elucidate mechanisms of stem cell function in their respective tissues and rescue/prevent age-related dysfunction.
PhD, University of South Carolina, Columbia, SC
Caloric Restriction and tissue resilience
Caloric restriction (CR) without malnutrition has been shown to extend lifespan with associated increase in tissue resilience. In skeletal muscle, short-term (3 month) CR increases muscle stem cell (satellite cell) number and regenerative function in both young and old mice. Much of these beneficial effects have been hypothesized to be mediated by secreted proteins. However, the identity of these proteins is largely unknown due, in part, to limited detection methods of the protein secretome. To get around these limitations, we have used the Albumin-Cre/MetRS model to characterize the CR-associated liver secretome. We have identified several differentially expressed proteins including plasminogen, a multifunctional zymogen well known to regulate hemostasis and more recently shown to play a role in tissue regeneration, including skeletal muscle.
METRNL improves aged muscle regenerations
Meteorin-like (or METRNL) is a cytokine that is secreted by inflammatory immune cells during the early stages of the regenerative process. Our lab published evidence in Nature Metabolism in 2020 of the necessity of METRNL during muscle regeneration. We are actively expanding upon these findings by investigating chronic disease states that present with insufficient levels of METRNL in response to injury. We are keenly interested in the physiological loss of METRNL secretion by aged macrophage populations in the muscle and how the response to METRNL interacts with other interstitial cell types to combat pathological muscle regeneration.
Muscle Stem (Satellite) Cell metabolism
Glutamine is one of the most active sources of carbon substrate used to generate energy in mitochondrial oxidative phosphorylation next to pyruvate and palmitate. We are actively investigating the important role of glutamine metabolism is the population of interstitial muscle stem cells that contribute to muscle’s regenerative capacity. By limiting metabolic shunting away from glutamine metabolism and enhancing the energy available to the muscle stem cell during its activation, we hope to maintain the resilience of muscle in models of aging.