Grant: Discovery Grants Program - Individual
University of Western Ontario
$34,000.00
ß1-integrin is a crucial regulator of the exocytotic machinery in pancreatic beta-cells, affecting insulin secretion and integrin trafficking.
EF 2018-19
Résumé
The discovery of insulin in 1921 by Banting and Best laid the foundation for the modern management of diabetes mellitus, a disease that affects millions of Canadians and costs our healthcare system more than $17 billion annually. However, insulin treatment cannot cure diabetes and will not prevent the secondary complications, which are responsible for the devastating morbidity and mortality of this disease. Replacement of insulin-producing (beta) cells through a cell-based therapy (e.g. pancreatic islet transplantation or a bioartificial endocrine pancreas) has the best chance to prevent, reverse or stabilize these complications. However, the scarcity of islets and limitations in our knowledge of the factors influencing islet biology present a major obstacle to the adoption of cell-based therapies as a routine treatment. Advancement in this field requires a thorough understanding of the factors that regulate growth of the islet beta cells and maintain their viability and function. *Our previous in vivo and in vitro studies have determined that the interactions of a beta cell receptor, 1-integrin, with extracellular matrix (ECM) proteins are essential for maintaining beta cell function and preventing cell death. Recently we discovered that the loss of 1 integrin in beta cells led to abnormalities in the insulin secretory pathway, including changes in the expression of specific secretory pathway proteins. In addition, alternative members of the integrin receptor family were expressed. As a result, our new research objectives are twofold: (1) to investigate how 1-ECM interactions regulate the expression of secretory pathway proteins in beta cells; and (2) to determine how 1-ECM interactions and the secretory pathway proteins influence which integrins are expressed in beta cells. *We believe that these studies will facilitate the development of appropriate tissue engineering strategies for a bioartificial endocrine pancreas. Such a treatment would have far-reaching economic and social benefits. *
Programme
Discovery Grants Program - Individual
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
NSERC's Awards Data
Tel que publié
Application id
RGPIN-2017-04658
Name nom
Wang, Rennian
Department département
Physiology and Pharmacology
Organization id
36
Institution établissement
University of Western Ontario
Province en
Ontario
Province fr
Ontario
Country en
CANADA
Country fr
CANADA
Fiscal year exercice financier
2018
Competition year année de concours
2017
Award amount
34000
Program id
RGPIN
Program name en
Discovery Grants Program - Individual
Program name fr
Programme de subventions à la découverte - individuelles
Group en
Discovery grants programs
Group fr
Programmes de subventions à la découverte
Committee code
1501
Committee name en
Genes, Cells and Molecules
Committee name fr
Gènes, cellules et molécules
Area of application code
1102
Area of application group en
Health, education and social services
Area of application group fr
Santé publique, éducation et services sociaux
Area of application en
Biomedical engineering
Area of application fr
Génie biomédical
Research subject code
5107
Research subject group en
Cell biology
Research subject group fr
Biologie cellulaire
Research subject en
Cell secretion
Research subject fr
Sécrétions cellulaires
Partie
2
Nb partie
5
Application title
ß1-integrin is a crucial regulator of the exocytotic machinery in pancreatic beta-cells, affecting insulin secretion and integrin trafficking.
Keyword
NSERC
Application summary
The discovery of insulin in 1921 by Banting and Best laid the foundation for the modern management of diabetes mellitus, a disease that affects millions of Canadians and costs our healthcare system more than $17 billion annually. However, insulin treatment cannot cure diabetes and will not prevent the secondary complications, which are responsible for the devastating morbidity and mortality of this disease. Replacement of insulin-producing (beta) cells through a cell-based therapy (e.g. pancreatic islet transplantation or a bioartificial endocrine pancreas) has the best chance to prevent, reverse or stabilize these complications. However, the scarcity of islets and limitations in our knowledge of the factors influencing islet biology present a major obstacle to the adoption of cell-based therapies as a routine treatment. Advancement in this field requires a thorough understanding of the factors that regulate growth of the islet beta cells and maintain their viability and function. *Our previous in vivo and in vitro studies have determined that the interactions of a beta cell receptor, 1-integrin, with extracellular matrix (ECM) proteins are essential for maintaining beta cell function and preventing cell death. Recently we discovered that the loss of 1 integrin in beta cells led to abnormalities in the insulin secretory pathway, including changes in the expression of specific secretory pathway proteins. In addition, alternative members of the integrin receptor family were expressed. As a result, our new research objectives are twofold: (1) to investigate how 1-ECM interactions regulate the expression of secretory pathway proteins in beta cells; and (2) to determine how 1-ECM interactions and the secretory pathway proteins influence which integrins are expressed in beta cells. *We believe that these studies will facilitate the development of appropriate tissue engineering strategies for a bioartificial endocrine pancreas. Such a treatment would have far-reaching economic and social benefits. *
