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Michael John Parsons, Ph.D.
Associate Professor of Surgery
Research Interests: therapeutic routes to treat diabetes
Michael Parsons, Ph.D., is an associate professor of surgery in the McKusick-Nathans Institute of Genetic Medicineand in the Johns Hopkins Department of Surgery.
He holds a bachelor’s degree in biology from the University of York and completed a Ph.D in anatomy and developmental biology from the University College London. Dr. Parsons completed a postdoctoral fellowship in 2002, where he focused on the positional cloning of genes required for development of the zebrafish notochord.
He has since presented his research findings at myriad international conferences, including the eighth European Zebrafish Meeting and the ninth International Meeting on Zebrafish Development and Genetics. Dr. Parsons previously served as the principal scientist in the Department of Comparative Genomics for GlaxoSmithKline, where he generated and managed a portfolio of mouse transgenic projects, before joining the Johns Hopkins faculty in 2004.
- Associate Professor of Surgery
Departments / Divisions
- Surgery - Surgical Oncology
Centers & Institutes
- B.Sc., York University (England) (1993)
- Ph.D., University College London (England) (1997)
MRC National Institute for Medical Research, London, London, United Kingdom, 2002, Project concerned the positional cloning of several genes required for correct development of the zebrafish notochord
Research & Publications
Diabetes is associated with a loss of insulin-producing β cells. In our quest to find therapeutic routes to treat diabetes, we aim to discover molecular and cellular mechanisms involved in β-cell neogenesis and regeneration. To do this we use a variety of transgenic and molecular tools to study the events that occur during development of the pancreas and its recovery from tissue damage.
Zebrafish as a Model System:
We utilize the zebrafish as a model system in order to expedite the discovery of mechanisms of β-cell neogenesis and regeneration. What makes the zebrafish particularly compelling for such research is that, unlike in mammals, zebrafish pancreatic cells readily regenerate following damage. Having established the pathways utilized by the fish in β-cell regeneration, we hope to pharmacologically induce the same pathways in human tissues.
Zebrafish are an ideal system to study vertebrate embryogenesis, being genetically tractable and having transparent, externally developing embryos. Easy transgenesis allows specific cells and their behaviors to be visualized within living animals. Moreover, with their small size and high fecundity, the zebrafish represents the only tangible method to perform high-throughput chemical screening on a living, intact vertebrate organism. Within a collaborative effort at Johns Hopkins, we have carried out two chemical screens to find compounds and pathways that influence β-cell biology.
Current Lab Projects:
- Assessing the role of CACs in pancreas regeneration.
- Using results from our chemical screens to improve protocols to make human β cells in vitro from embryonic stem cells.
- Using genomics-based approaches to examine the function of the transcription factor SOX9 in pancreatic progenitors.
- Exploring the pancreatic phenotype in CFTR loss of function zebrafish.
- Testing the role of neuromodulators on β-cell development and biology.
Selected PublicationsView all on Pubmed
- Wang YJ, Park JT, Parsons MJ and Leach SD. Fate mapping of ptf1a-expressing cells during pancreatic organogenesis and regeneration in zebrafish. Developmental Dynamics (accepted)
- Huang W, Wang G, Delaspre F, Vitery MD, Beer RL, Parsons MJ. Retinoic acid plays an evolutionarily conserved and biphasic role in pancreas development. Developmental Biology. 394, pp 83-93.
- Park JT, Johnson N, Liu S, Levesque M, Wang YJ, Ho H, Huso D, Maitra A, Parsons MJ, Prescott JD, Leach SD. Differential in vivo tumorigenicity of diverse KRAS mutations in vertebrate pancreas: A comprehensive survey. Oncogene. doi: 10.1038/onc.2014.223.
- Quillien A, Moore JC, Shin M, Siekmann AF, Smith T, Pan L, Moens CB, Parsons MJ, Lawson ND. Distinct Notch signaling outputs pattern the developing arterial system.
- Development. 141(7), pp 1544-52.
- Adoption of the Q transcriptional regulatory system for zebrafish transgenesis. Subedi A, Macurak M, Gee ST, Monge E, Goll MG, Potter CJ, Parsons MJ, Halpern ME. Methods. 66(3), pp433-40.
- Aldh1-expressing endocrine progenitor cells regulate secondary islet formation in larval zebrafish pancreas. Matsuda H, Parsons MJ, Leach SD. PLoS One. 17;8(9):e74350. doi: 10.1371/journal.pone.0074350.