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Maureen Gannon, Ph.D.
Associate Professor

Department of Medicine, Division of Diabetes, Endocrinology and Metabolism


Department of Molecular Physiology and Biophysics

Department of Cell and Developmental Biology

Vanderbilt University Medical Center
2213 Garland Avenue
MRB IV 7435
Nashville, TN 37232

office: (615) 936-2676    
lab: (615) 936-2683        
fax: (615) 936-1667

Gannon Lab Home

Gannon Lab 2013


Research Interests


The pancreas is essential for normal digestion and maintenance of blood sugar levels. It is composed of an exocrine compartment, made up of acinar and ductal cells that secrete and transport digestive enzymes, as well as an endocrine compartment (the Islets of Langerhans), made up of alpha cells that produce glucagon, beta cells that produce insulin, delta cells that produce somatostatin, and PP cells that produce pancreatic polypeptide.
 

We study the role of genes and signaling pathways involved in the development and function of specific cell types within the pancreas.

 

 Ackermann and Gannon, (2007) J. Mol. Endocrinology

 

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 have 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 pancraetitis and pre-neoplastic lesions. Current studies are examining how HNF6 interacts with other factors in the embryonic pancreas to regulate endocrine differentiation.

 


Guney and Gannon, (2009) Embryo Today: Reviews

 

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.

 


 Crawford and Guney et al. Mol. Endocrinology, 2009
 

Finally, the FoxM1 transcription factor is highly expressed in proliferating cells and is essential for normal cell division. We have 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 have 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 FoxM1 mutants, 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 identifying target genes of FoxM1 in the insulin-producing cells.

 

 Ackermann and Gannon, (2007) J. Mol. Endocrinology

 

 

Area of Research: Molecular and cell biology of pancreas development and function

Research Key Words: mouse, developmental biology, molecular genetics of pancreas development, organogenesis, morphogenesis, islet function, beta cell, diabetes, transcription factor, knockout, transgenic, mutation, stem cell

 

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This page was last updated April 10, 2013 and is maintained by Maureen Gannon