We specialize in understanding mechanisms regulating gut homeostasis in health and disease with a specific interest in how epithelial cells respond to damage and inflammation. We employ in vivo models and 3D organoid cultures (enteroids, colonoids) from mice and humans to understand the molecular and cellular basis of tissue regeneration and inflammatory bowel disease (IBD). Within these contexts, we study how RNA-binding proteins impart post-transcriptional regulation of key pathways in normal physiology and disease.

Post-transcriptional control of intestinal epithelial healing

Gene expression regulation can happen at multiple levels. We aim to understand how post-transcriptional mechanisms (i.e. mechanisms regulating RNA -> protein) direct the cell to respond and adapt to changes in the environment. We focused recently on post-transcriptional regulation of the autophagy pathway. Understanding post-transcriptional regulation of key cellular pathways, such as autophagy, in the context of disease allows us to better define how normal cells behave and will provide a foundation for developing new therapies or augmenting existing therapies for diseases including inflammatory bowel disease.

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Epithelial cell contributions to the pathogenesis of IBD

Our laboratory uses 3D organoids (enteroids and colonoids) from patients with inflammatory bowel disease (IBD) and compares them to healthy patients to understand how intestinal epithelial cells contribute to disease severity. Our recent focus has been on studying Very Early Onset (VEO)-IBD, which represents a subset of pediatric IBD patients with severe disease. Our hope is to use enteroid/colonoid technology to understand multiple areas, including: 1) how epithelial cells from different patients grow and renew; 2) how different patients respond to current therapies; and 3) to test new therapies for patients in which current strategies aren't effective.