Grant: Travel Awards - Institute Community Support
McGill University
$1,500.00
Podocyte-Specific Hyper-Activation of Rac1 Induces Glomerulosclerosis and Nephrotic Syndrome
EF 2014-15
Résumé
The main function of the kidneys is to filter the blood of waste products and produce urine. Within the kidneys are millions of
glomeruli (singular:glomerulus) which are the sites where urine formation begins. The glomerulus functions as a filtration barrier that prevents the loss of important blood proteins into the urine. Nephrotic Syndrome (NS) is a disorder of the kidney
in which this filtration barrier is damaged and blood proteins are lost into the urine. It is common among children. The consequences
of heavy protein loss can include edema (swelling), infections, blood clots and in severe cases, the need for dialysis or kidney transplantation to halt the protein loss.The kidney's filtration barrier contains a population of cells known as podocytes that are necessary for filtration function. Podocytes have a unique three-dimensional architecture with numerous small
projections called foot processes that wrap around blood vessels, thereby blocking protein spillage into the urine. A family of proteins
called Rho-GTPases regulate the three dimensional architecture of podocytes. The protein known as Rac1, is a key member of the Rho-GTPase family and it is necessary to maintain the three dimensional architecture of podocytes and for them to function properly. It is important that Rac1 activity is properly regulated in podocytes. We have genetically engineered experimental mice that express a hyper-active mutant form of Rac1 specifically within podocytes. When the hyper-active Rac1 is induced in these mice, they exhibit protein loss in the urine, kidney scarring and other problems associated with diseases of the glomerulus.
We propose to study in detail how Rac1 affects the health of podocytes and how this protein can be targeted to treat NS, thereby improving the quality of the lives of people afflicted with the disease.
Programme
Travel Awards - Institute Community Support
Bénéficiaire
Emplacement
Quebec, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
315405
Name
Robins Richard
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Genetics
Theme2
Biomedical
Prcname2
Institute of Nutrition, Metabolism and Diabetes
Projecttitle
Podocyte-Specific Hyper-Activation of Rac1 Induces Glomerulosclerosis and Nephrotic Syndrome
Programtype2
Undefined
Orgnameinp2
McGill University
Cihramount2
$1,500
Cihrequipment2
$0
Programname2
Travel Awards - Institute Community Support
Keyworddelim
Nephrotic Syndrome; Podocytes; Rac1
Abstract
The main function of the kidneys is to filter the blood of waste products and produce urine. Within the kidneys are millions of
glomeruli (singular:glomerulus) which are the sites where urine formation begins. The glomerulus functions as a filtration barrier that prevents the loss of important blood proteins into the urine. Nephrotic Syndrome (NS) is a disorder of the kidney
in which this filtration barrier is damaged and blood proteins are lost into the urine. It is common among children. The consequences
of heavy protein loss can include edema (swelling), infections, blood clots and in severe cases, the need for dialysis or kidney transplantation to halt the protein loss.The kidney's filtration barrier contains a population of cells known as podocytes that are necessary for filtration function. Podocytes have a unique three-dimensional architecture with numerous small
projections called foot processes that wrap around blood vessels, thereby blocking protein spillage into the urine. A family of proteins
called Rho-GTPases regulate the three dimensional architecture of podocytes. The protein known as Rac1, is a key member of the Rho-GTPase family and it is necessary to maintain the three dimensional architecture of podocytes and for them to function properly. It is important that Rac1 activity is properly regulated in podocytes. We have genetically engineered experimental mice that express a hyper-active mutant form of Rac1 specifically within podocytes. When the hyper-active Rac1 is induced in these mice, they exhibit protein loss in the urine, kidney scarring and other problems associated with diseases of the glomerulus.
We propose to study in detail how Rac1 affects the health of podocytes and how this protein can be targeted to treat NS, thereby improving the quality of the lives of people afflicted with the disease.
Competitiondate
201409
Approvedterm2
1 yr 0 mth
Pinamesdelim
Robins, Richard
Approvedterm
1 an 0 mois
Cihrcontribution2
Inst of Nutr Metabolism &Diab~ $1,500~ $0~