The Hilton Lab research interests are aimed at uncovering the molecular circuitry regulating lineage commitment, proliferation, and differentiation of skeletal stem and progenitor cells (SSPCs), chondrocytes, osteoblasts, myoblasts, and non-myogenic mesenchymal cells within skeletal muscle, some of which are known as fibro-adipogenic progenitors (FAPs). My laboratory utilizes intricate surgical and genetic mouse models, biochemical approaches, and primary tissue/cell culture techniques to investigate the underlying tissue, cellular, and molecular mechanisms responsible for musculoskeletal development, disease, and regeneration. My lab has been particularly focused on the role of cell signaling mechanisms that influence these processes in both cell autonomous and non-autonomous manners.
A multitude of cellular signaling pathways are required during normal muscle, bone, and cartilage development. Deregulation of these signaling circuits result in a variety of skeletal dysplasias, muscular dystrophies, and other muscle disorders. Through the use of sophisticated mouse genetic approaches and complex cellular and molecular techniques, we aim to understand the signaling mechanisms that regulate cell and stem cell proliferation, differentiation, fate determination, and self renewal during musculoskeletal development .
We study various musculoskeletal diseases that include: osteoarthritis (OA), osteoporosis, and the muscular dystrophies. Our laboratory has a particular interests in the genetics that underlie normal maintenance and pathological joint degeneration and pain associated with OA, the skeletal stem and progenitor cell (SSPC) dysregulation that leads to osteoporosis and low bone mass, as well as the dysfunction of non-myogenic mesenchymal cells implicated in muscle disease. We employ both genetic and surgical mouse models and sophisticated cell and molecular analyses to understand the pathologies associated with all of these musculoskeletal diseases.
Damaged tissue from musculoskeletal injuries, such as bone fractures critical sized bone defects, or rotator cuff tears, often make some attempt to repair or regenerate via mechanisms that are similar to processes involved in musculoskeletal development. Our laboratory is interested in uncovering the role that various cell or stem cell populations and signaling pathways play in musculoskeletal tissue regeneration. We are using genetic, surgical, and molecular approaches to understand the processes involved in musculoskeletal regeneration, while developing approaches to enhance or accelerate muscloskeletal regeneration.