Diane E. Peters, DVM, MS, PhD
Highlights
Languages
- English
Gender
FemaleJohns Hopkins Affiliations:
- Johns Hopkins School of Medicine Faculty
About Diane E. Peters
Primary Academic Title
Assistant Professor of Pharmacology and Molecular Sciences
Background
Dr. Diane E. Peters is an Assistant Professor in the Department of Pharmacology and Molecular Sciences, and a member of the Johns Hopkins Drug Discovery Pharmacology Division.
Dr. Peters received her Ph.D. in Pharmacology and Experimental Therapeutics from the Tufts University Graduate School of Biomedical Sciences. She then pursued advanced training in comparative medicine, receiving both an M.S. in Laboratory Animal Medicine and a D.V.M. from the Tufts University Cummings School of Veterinary Medicine, and performing a research fellowship in Laboratory Animal Medicine at the Johns Hopkins University School of Medicine.
Dr. Peters applies her dual veterinary and pharmacology expertise towards preclinical drug discovery efforts, with a focus on the development of novel treatments for inflammatory bowel disease.
Research Interests
Biomarker Validation, Drug Discovery, In vivo Pharmacology/Toxicology, Inflammatory Bowel Disease, Preclinical Model Characterization
Research Summary
The Peters lab applies a translational medicine approach to study the pathobiology of inflammatory bowel disease (IBD), with the ultimate goal of developing mechanistically novel IBD therapeutics. Our laboratory uses preclinical rodent colitis models and genetically modified mice to characterize pathways involved in inflammation and pain in IBD, with validation of all findings in human patient samples. We employ molecular pharmacology to interrogate pathways critical to colitis initiation and progression, and work closely with Johns Hopkins Drug Discovery to develop rationally-designed small molecule drugs targeting pathways of interest.
Current efforts in the lab include the development of small molecule glutamate carboxypeptidase (GCPII) inhibitors for use in IBD. GCPII is an enzyme that is highly and specifically upregulated in IBD and we, and others, have shown that GCPII inhibitors protect mice from developing colitis. Expanding on this finding, ongoing activities in our lab include validating GCPII as a clinical biomarker in defined IBD patient populations, exploring the biology of GCPII in the colon, and profiling mechanism(s) of actions of GCPII inhibitors in colitis.