The immediate interruption of the bone marrow microenvironment during long bone trauma activates local erythropoiesis. Erythroid progenitors have been described to direct iron and oxygen metabolism. We study how erythroid progenitors direct the local metabolic and immune microenvironment instructing regeneration during fracture repair.

Cartilage is avascular and requires a hypoxic niche to maintain proper metabolism and matrix integrity. Oxygen diffuses from the synovial fluid into the cartilage matrix. We elucidate dynamic intra- and extracellular oxygen signatures in cartilage, synovial fluid, and synovial membrane in vivo during post-traumatic OA and hemarthrosis. 

We leverage fundamental knowledge to develop novel, programmable biomaterials by engineering microenvironmental cues to guide erythroid stem cell fate and by targeting cellular oxygen to re-establish the hypoxic cartilage niche for tissue restoration.