G protein-coupled receptor kinase 3 modulates mesenchymal stem cell proliferation and differentiation through sphingosine-1-phosphate receptor regulation.

A long-term interest of the Hilton lab is to uncover the molecular circuitry regulating lineage commitment, proliferation, and differentiation of skeletal stem cells, chondrocytes, and osteoblasts. My laboratory uses genetic mouse models and primary cell culture techniques coupled with biochemistry to answer questions regarding skeletal stem cell self-renewal/differentiation, chondrogenesis, and osteoblastogenesis. Recently my lab has generated novel data from a variety of Notch gain and loss-of-function mutant mice demonstrating the importance of Notch signaling in each of these processes. We are currently investigating the exact Notch signaling mechanisms at play during skeletal development, disease, and repair. Additional studies are also focused on identifying and understanding the molecular mechanisms underlying various congenital skeletal pathologies, including Multiple Herediatry Exostoses (MHE) and Preaxial Polydactyly (PPD).

I first became interested in clinical immunology as a medical student studying autoimmune inflammatory eye disease at the National Institutes of Health.  Since then, I have been inspired to understand what causes autoimmunity and immune deficiency disorders in order to improve the quality of life for my patients.  I see patients with multiple complex immune disorders with particular expertise in autoimmune and Rheumatoid arthritis, primary Sjogren's syndrome, and the immunodeficiency disorders Common Variable Immunodeficiency (CVID), Adenosine Deaminase Deficiency (ADA) disorders, and WHIM (Warts, Hypogammaglobulinemia, Infections, and Myelokathexis). My research investigates immune targets that may impact either the development of immune disease or identify new therapies for patients.  The goal is to help us understand why and how immunologic diseases develop so that we may better treat them.