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Maureen Gannon, Ph.D.
Professor
Department of Medicine, Division of Diabetes, Endocrinology, and Metabolism
Department of Molecular Physiology and Biophysics
Department of Cell and Developmental Biology
Vice Chair for Faculty Development
DRTC, Director of Enrichment, Training and Outreach
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National Institutes of Health Women Scientists

The NIH Working Group on Women in Biomedical Careers is a trans-NIH effort to consider barriers for women in science and to develop innovative strategies to promote entry, recruitment, retention, and sustained advancement of women in biomedical and research careers.

Research Specialty: 
Our laboratory studies genes that regulate pancreatic beta cell mass, that is, the number of insulin-producing cells that an organism has. We study genes that control the formation of beta cells in the embryo and also genes that regulate the increase in beta cell number in response to environmental cues such as pregnancy and increased weight gain.

Gannon Lab »

Research Description:
The pancreas is essential for normal digestion and maintenance of blood sugar levels. We study the role of genes and signaling pathways involved in the development and function of specific cell types within the pancreas. The HNF6 transcription factor is expressed in all pancreas cells early in embryonic development, but is "turned off" in islet cells just before birth in the mouse. We developed mice in which HNF6 can be inactivated conditionally in different cell types. These studies reveal that HNF6 is essential to generate the appropriate number of endocrine progenitor cells, and that HNF6 is essential for branching of the pancreatic ductal epithelium and for duct cell differentiation. In the absence of HNF6, pancreatic duct differentiation is impaired and the mice develop pancreatitis and pre-neoplastic lesions. Current studies are examining how HNF6 interacts with other factors in the embryonic pancreas to regulateendocrine differentiation.

A second project in the lab examines the role of CTGF, a secreted factor known to modulate growth factor signaling. We found that loss of CTGF results in decreased embryonic islet beta cell proliferation and defective islet formation. Using conditional gene inactivation and over-expression strategies we also found that CTGF is critical for islet vascularization and can increase beta cell proliferation and islet mass. We are currently examining whether CTGF can improve islet transplantation outcomes and in vivo beta cell regeneration as potential cures for diabetes. Finally, the FoxM1 transcription factor is highly expressed in proliferating cells and is essential for normal cell division. We generated mice lacking FoxM1 in the pancreas. In these mice, the number of insulin-producing cells fails to increase with body mass, resulting in diabetes. Significantly, we found that FoxM1 is required downstream of all proliferative stimuli in the insulin-producing beta cells. For example, the number of beta cells expands via mitosis when animals are fed a high fat diet, or during pregnancy. In FoxM1mutants, this increase in mitosis does not occur and the animals become diabetic. Our current studies are aimed at characterizing the signaling pathways that activate FoxM1 expression and activity as well as identifyingtarget genes of FoxM1 in the insulin-producing cells.