Grant: Operating Grant
University of Toronto
$574,358.00
The Role of Discoidin Domain Receptor 1 (DDR1) in Vascular Calcification of Atherosclerosis and Diabetes
FY 2013-14
Summary
Calcification of arteries occurs in more than 1/2 of the population over the age of 60, and causes significant complications in vascular diseases like atherosclerosis, diabetes and hypertension. Minerals are deposited in the matrix surrounding cells in blood vessels, and this causes thickening, stiffening and sometimes rupture of these vessels. We have recently discovered that a matrix receptor protein which is expressed on arterial smooth muscle cells is involved in the deposition of minerals. This receptor, DDR1, causes a switch in the smooth muscle cells so that they start to behave like bone cells. We hope to better understand the role of DDR1 in these processes, and the consequences for normal function of blood vessels. Our work may lead to the development of new therapies designed to inactivate DDR1 and therefore prevent the calcification of arteries.
Department
Program
Operating Grant
Recipient
Location
Ontario, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
290609
Name
Bendeck Michelle P
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Cardiovascular System - B: Heart and Circulation
Projecttitle
The Role of Discoidin Domain Receptor 1 (DDR1) in Vascular Calcification of Atherosclerosis and Diabetes
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$574,358
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Atherosclerosis; Diabetes; Discoidin Domain Receptor; Extracellular Matrix; Intracellular Signaling; Mechanotransduction; Transgenic Mice; Vascular Calcification
Abstract
Calcification of arteries occurs in more than 1/2 of the population over the age of 60, and causes significant complications in vascular diseases like atherosclerosis, diabetes and hypertension. Minerals are deposited in the matrix surrounding cells in blood vessels, and this causes thickening, stiffening and sometimes rupture of these vessels. We have recently discovered that a matrix receptor protein which is expressed on arterial smooth muscle cells is involved in the deposition of minerals. This receptor, DDR1, causes a switch in the smooth muscle cells so that they start to behave like bone cells. We hope to better understand the role of DDR1 in these processes, and the consequences for normal function of blood vessels. Our work may lead to the development of new therapies designed to inactivate DDR1 and therefore prevent the calcification of arteries.
Competitiondate
201309
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Bendeck, Michelle P
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $574,358~ $0~
