In response to RFA-DK-09-504 we present a plan for future activities of the Coordinating Center for the Beta Cell Biology Consortium (BCBC). This consortium, which was initially launched in September 2001 then renewed in 2005, brings a team-oriented approach to studies necessary to learn how to regenerate or replace pancreatic beta cells that are either destroyed or damaged by Type 1 or Type 2 diabetes. The Coordinating Center plays a vital role in the consortium by 1) organizing investigator meetings and retreats, 2) maintaining the BCBC website and reagent databases, 3) overseeing BCBC core facilities, 4) providing advanced bio/informatics applications, 5) managing special funding programs, 6) providing various types of administrative support, and 7) facilitating interactions with other NIH-sponsored Centers and Consortia. During the next cycle of the BCBC the Coordinating Center will 1) continue to perform many ongoing operations, 2) adapt to changes in the scientific focus and new participants, and 3) improve the website in a way to facilitate team science and sharing of unpublished knowledge and reagents.

Public Health Relevance

Type 1 and Type 2 diabetes cause significant morbidity and mortality and thus have an adverse economic impact. Both diseases are characterized by the destruction or dysfunction of insulin-secreting pancreatic beta cells. This application will coordinate activities among a team of scientists in order to develop new, cell-based replacement therapies that hold promise for achieving better glucose control than is currently possible.

Agency
National Institute of Health (NIH)
Institute
National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
Type
Research Project--Cooperative Agreements (U01)
Project #
5U01DK072473-08
Application #
8326734
Study Section
Special Emphasis Panel (ZDK1-GRB-G (M3))
Program Officer
Sato, Sheryl M
Project Start
2005-08-01
Project End
2015-07-31
Budget Start
2012-08-01
Budget End
2013-07-31
Support Year
8
Fiscal Year
2012
Total Cost
$3,699,999
Indirect Cost
$640,769
Name
Vanderbilt University Medical Center
Department
Physiology
Type
Schools of Medicine
DUNS #
004413456
City
Nashville
State
TN
Country
United States
Zip Code
37212
Saunders, Diane C; Brissova, Marcela; Phillips, Neil et al. (2018) Ectonucleoside Triphosphate Diphosphohydrolase-3 Antibody Targets Adult Human Pancreatic ? Cells for In Vitro and In Vivo Analysis. Cell Metab :
Hart, Nathaniel J; Aramandla, Radhika; Poffenberger, Gregory et al. (2018) Cystic fibrosis-related diabetes is caused by islet loss and inflammation. JCI Insight 3:
Fowler, Jonas L; Lee, Steve Seung-Young; Wesner, Zachary C et al. (2018) Three-Dimensional Analysis of the Human Pancreas. Endocrinology 159:1393-1400
Sui, Lina; Danzl, Nichole; Campbell, Sean R et al. (2018) ?-Cell Replacement in Mice Using Human Type 1 Diabetes Nuclear Transfer Embryonic Stem Cells. Diabetes 67:26-35
Gutierrez-Martinez, Paula; Hogdal, Leah; Nagai, Manavi et al. (2018) Diminished apoptotic priming and ATM signalling confer a survival advantage onto aged haematopoietic stem cells in response to DNA damage. Nat Cell Biol 20:413-421
Cigliola, Valentina; Ghila, Luiza; Thorel, Fabrizio et al. (2018) Pancreatic islet-autonomous insulin and smoothened-mediated signalling modulate identity changes of glucagon+ ?-cells. Nat Cell Biol 20:1267-1277
Olehnik, Scott K; Fowler, Jonas L; Avramovich, Gil et al. (2017) Quantitative analysis of intra- and inter-individual variability of human beta-cell mass. Sci Rep 7:16398
Aamodt, Kristie I; Powers, Alvin C (2017) Signals in the pancreatic islet microenvironment influence ?-cell proliferation. Diabetes Obes Metab 19 Suppl 1:124-136
Stancill, Jennifer S; Cartailler, Jean-Philippe; Clayton, Hannah W et al. (2017) Chronic ?-Cell Depolarization Impairs ?-Cell Identity by Disrupting a Network of Ca2+-Regulated Genes. Diabetes 66:2175-2187
Yang, Yu-Ping; Magnuson, Mark A; Stein, Roland et al. (2017) The mammal-specific Pdx1 Area II enhancer has multiple essential functions in early endocrine cell specification and postnatal ?-cell maturation. Development 144:248-257

Showing the most recent 10 out of 144 publications