Lysosomal acid lipase (LAL) hydrolyzes cholesteryl esters and triglycerides to generate free fatty acid and cholesterol in the lysosomes of various cells. The metabolites of the enzyme product serve as ligands for nuclear receptors and transcription factors that regulate gene expression, cell proliferation/differentiation and apoptosis. The physiological roles of LAL are evaluated using a gene targeted mouse model, LAL knock out mice (lal-/-) that created in my laboratory. Further characterization of lal-/- mice demonstrated additional roles of LAL in fat mobilization, insulin resistance, myeloid cell and T cell dysfunction, respiratory inflammation and remodeling. Our current research focuses on mechanisms that connect lipid metabolism disorder to the systemic inflammation that leads to multiple forms of pathogenic phenotypes in multiple organs.
Post-doctoral Fellowship - The Rockefeller University, New York 1989-1992
Ph.D. - City University of New York, New York 1989
