Our group studies the transcriptional regulation of skeletal & cardiac muscle genes by identifying their enhancers, promoters, DNA control elements, and transcription factors. This basic information is then used for designing miniaturized Muscle-Specific Expression Cassettes (MSECs) for gene therapy treatments of Neuromuscular & Cardiac muscle diseases. MSECs are optimized via the design and testing of transcription factor DNA binding site arrays capable of synthesizing muscle type-specific therapeutic product levels that are maximally beneficial for treating each disease.
Bone and muscle mass are strongly coupled, as evidenced by the fact that osteoporosis and sarcopenia frequently occur in the same individual, a condition termed osteosarcopenia. With support from the CTMR, our lab is determining the biological mechanisms underlying genetic risk for osteosarcopenia in order to develop new approaches for its diagnosis and treatment.
We use molecular, biomechanical and computational approaches to study pathogenesis of acquired and genetic muscle disorders. We are interested in precision medicine and novel sarcomeric-based therapies. The experimental approaches used in our group span from recombinant proteins and isolated myosin motors to myofibrils, multicellular preparation, cells and whole organ analysis. The computational approaches in the lab include multi-scale model of the sarcomere and large data analytics.
A primary objective of the Odom lab at the University of Washington is to develop improved therapies for Duchenne Muscular Dystrophy (DMD). CTMR core facilities have provided a unique mechanism to enhance our capacity for generating high quality critical data with regard to muscle metabolism and biomechanics. One ongoing research project pursues a potential synergy between two promising gene therapy approaches toward ameliorating cardiopulmonary performance in preclinical models of DMD. In this project we address the underlying genetic defect of DMD (the lack of dystrophin) by protecting myofibers from further injury via AAV-mediated delivery of micro-dystrophin while simultaneously improving the relative magnitude & rate of cardiac contractility via alternative nucleotide therapy (ribonucleotide reductase) with ionotropic enhancement, potentially providing for a unique therapeutic advantage.
Kat M. Steele is the Albert S. Kobayashi Endowed Professor in Mechanical Engineering. Her work combines musculoskeletal simulation, biomechanical assessments, clinical trials, and inclusive design to improve mobility for individuals with neurological disorders. Current work includes understanding how muscle impairments, such as spasticity, contracture, and weakness impact mobility after brain injury, and investigation of new interventions (i.e., exoskeletons, spinal stimulation, mobility aids) can improve participation and quality of life.