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Michele T. Pritchard, Ph.D.

Michele Pritchard portrait
Associate Professor, Pharmacology, Toxicology & Therapeutics

Professional Background

Postdoctoral Fellow, Nutritional Sciences, Case Western Reserve University, 2006
Postdoctoral Fellow, Pathobiology, Cleveland Clinic, 2008
Research Associate, Pathobiology, Cleveland Clinic, 2009
Project Scientist, Pathobiology, Cleveland Clinic, 2011
Assistant Professor, Gastroenterology and Liver Disease and Department of Pathology, Case Western Reserve University, 2012

Education and Training
  • BS, Biological Sciences, State University of New York at Buffalo
  • PhD, Tumor Immunology, State University of New York at Buffalo, Roswell Park Cancer Institute Graduate Division
  • Post Doctoral Fellowship, State University of New York at Buffalo, Roswell Park Cancer Institute Graduate Division, Department of Immunology
  • Post Doctoral Fellowship, CASE Western Reserve University, Department of Nutrition
  • Post Doctoral Fellowship, Cleveland Clinic, Department of Pathobiology
  • Other, Cleveland Clinic, Department of Pathobiology
Professional Affiliations
  • Society for the Study of Reproduction, Member, 2019 - Present
  • Society of Toxicology, Member, 2017 - Present
  • American Association for the Study of Liver Diseases, Member, 2013 - Present
  • International Society for Hyaluronan Sciences, Member, 2013 - Present
  • Research Society on Alcoholism, Member, 2010 - Present
  • International Society for Hepatic Sinusoidal Research, Member, 2009 - Present



I have a long-standing interest in inflammation: inflammation in tumors, inflammation in alcohol-associated liver disease, inflammation in liver regeneration and fibrosis, and inflammation in ovarian fibrosis associated with advanced reproductive age. What regulates inflammation and how to modulate inflammation to promote adaptive instead of maladaptive tissue responses to injury or aging remains an underdeveloped research area. While cytokines, chemokines, and cells of the innate immune system attract significant attention, how the extracellular matrix (ECM) regulates tissue inflammation and homeostasis has received considerably less attention; this is an active area of investigation by our research group. We are particularly interested in an ECM glycosaminoglycan named hyaluronan (HA). HA exerts dichotomous biological functions based on its molecular mass: high molecular mass HA is homeostatic and limits inflammation while low molecular mass HA promotes inflammation and fibrosis. We are leveraging this information to improve liver wound repair (i.e. prevent liver fibrosis and enhance liver regeneration). We are also using this information to prevent ovarian fibrosis associated with reproductive aging. The three active projects ongoing in the lab are as follows:

1. Homeostatic to reactive hyaluronan matrices in reproductive aging
2. Hyaluronan-mediated acceleration of alcohol-associated liver injury
3. Hyaluronan and regulation of liver regeneration

Current Research and Grants
  • Collaborative research: Hyaluronan, Nrf2 and protracted female fertility in long-lived, naked mole rats, NSF, Co-I
  • Briley, S., M, Jasti, S, McCracken, J., M, Hornick, J., E, Fegley, B, Pritchard, M., T, Duncan, F., E. 2016. Reproductive age-associated fibrosis in the stroma of the mammalian ovary.. Reproduction (Cambridge, England), 152 (3), 245-260
  • Deshpande, K., T, Liu, S, McCracken, J., M, Jiang, L, Gaw, T., E, Kaydo, L., N, Richard, Z., C, O'Neil, M., F, Pritchard, M., T. 2016. Moderate (2%, v/v) Ethanol Feeding Alters Hepatic Wound Healing after Acute Carbon Tetrachloride Exposure in Mice.. Biomolecules, 6 (1), 5
  • McCracken, J., M, Jiang, L, Deshpande, K., T, O'Neil, M., F, Pritchard, M., T. 2016. Differential effects of hyaluronan synthase 3 deficiency after acute vs chronic liver injury in mice.. Fibrogenesis & Tissue Repair, 9, 4
  • Pritchard, M., T, McCracken, J., M. 2015. Identifying Novel Targets for Treatment of Liver Fibrosis: What Can We Learn from Injured Tissues which Heal Without a Scar?. Current Drug Targets, 16 (12), 1332-46
  • Pritchard, M., T, McMullen, M., R, Stavitsky, A., B, Cohen, J., I, Lin, F, Edward Medof, M, Nagy, L., E. 2007. Differential contributions of C3, C5, and decay-accelerating factor to ethanol-induced fatty liver in mice.. Gastroenterology, 132 (3), 1117-1126
  • McMullen, M., R, Pritchard, M., T, Wang, Q, Millward, C., A, Croniger, C., M, Nagy, L., E. 2005. Early growth response-1 transcription factor is essential for ethanol-induced fatty liver injury in mice.. Gastroenterology, 128 (7), 2066-76