Liver is a primary site of macronutrient metabolism. Obesity linked diseases of the liver such as nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) result in ECM expansion, defective hormonal responses, and disrupted transcriptional networks. Integrin receptors and their immediate post-receptor pathways convert sensory inputs from the ECM to biochemical processes within the cell. Altered expression of several integrin signaling components accompanies the metabolic dysregulation that occurs in high fat (HF)-fed mice. The mechanisms linking ECM expansion and integrin signaling to metabolic disease are a primary focus of our lab. My research utilizes hepatocyte specific knockout of several integrin signaling components (e.g. integrin α5, integrin β1, and Integrin-linked kinase) in mice to fully characterize these pathways and their involvement in pathologic responses of the liver to high fat feeding.
Graduate Student, Wasserman laboratory, Molecular Physiology & Biophysics
823 Light Hall