Charles A. Harris, MD, PhD

Charles A. Harris, MD, PhD

Assistant Professor of Medicine


Charles Harris did his undergraduate studies at Brown University. He received his MD and PhD degrees from Washington University School of Medicine where he studied neuronal apoptosis in the laboratory of Eugene M Johnson Jr. Dr. Harris was the recipient of the O’Leary Prize in Neuroscience Research as well as the Needleman Prize in Pharmacology Research. Dr. Harris then did a residency in internal medicine at Barnes Hospital followed by Endocrinology fellowship training at UCSF. As a clinical fellow in endocrinology Dr. Harris became fascinated with Cushing’s syndrome of glucocorticoid excess, which led to his research focus on the molecular mechanisms for glucocorticoid action. While at UCSF, Dr. Harris was a research fellow in the laboratory of Robert V. Farese Jr. in the J. David Gladstone Institute for Cardiovascular Disease. Upon completing fellowship Dr. Harris was an Adjunct Assistant Professor of Medicine at UCSF and a Staff Scientist at the Gladstone Institutes. Dr. Harris is the recipient of the Endocrine Society Young Investigator Award (2011). Dr. Harris joined the faculty of the Department of Medicine at Washington University School of Medicine in 2013.

Research Interests

We are interested in the molecular mechanisms of glucocorticoid action. Glucocorticoids are stress hormones produced by the adrenal gland but are also used as medication to treat a wide variety of common inflammatory conditions such as asthma, inflammatory bowel disease and rheumatoid arthritis. Although glucocorticoids are potent and effective treatments for these conditions their use is limited due to severe side effects such as weight gain, diabetes/insulin resistance, hypertension, osteoporosis, myopathy as well as cognitive changes, a constellation of symptoms known as Cushing’s syndrome. We therefore hope to understand the site of action of glucocorticoids in manifesting these adverse effects. Central to this aim is a greater understanding of the glucocorticoid receptor, a member of the nuclear hormone receptor gene family. We currently use a spectrum of techniques from whole mouse physiology to cell biology to molecular biology. For our mouse studies, we use mice with quantitative alterations to both glucocorticoid ligand production (A Cushingoid transgenic mouse: the CRH-Tg mice or adrenalectomized mice) as well as GR signaling (whole knockout as well as tissue specific knockouts of GR). We also use mice with qualitative differences in GR signaling introduced by homologous recombination. We use a combination of traditional methods to study metabolism as well as cutting edge technologies including stable isotope mass spectrometry of whole mice to determine metabolic flux. For our cell-based studies we use mouse embryonic fobroblasts and adipocytes derived from these fibroblasts. These cells have the advantage of being primary cells that can be generated from a wide variety of genetically modified mice and are tractable to shRNA studies as well. We use a combination of cell culture and tissues from animals to perform whole-genome molecular approaches such as microarray and Chip-Seq to better understand molecular mechanisms of glucocorticoid action in physiologically relevant cell types.

Because of the prominent role of glucocorticoids on triacylglycerol metabolism and adipocyte biology, additional projects in the lab are focused on the triacylglycerol synthesis pathway, adipogenesis and adipocyte biology. A new project is the characterization of a novel adipocyte specific gene identified in one of our microarray experiments.

Harris Lab