Grant: Operating Grant
Centre hospitalier de l'Université de Montréal (CHUM)
$578,594.00
Characterization of non-classical protein secretion pathways of importance in renal fibrosis triggered by the paracrine apoptotic program
EF 2011-12
Résumé
Injury to the vessels providing blood supply to the kidneys leads to abnormal renal healing, a leading cause of renal failure. We found that dying vascular cells release Connective Tissue Growth Factor (CTGF), a mediator implicated in abnormal healing. Fibroblasts, cells present within the kidney, also produce increased amounts of CTGF when stressed. Here we plan to characterize the genes and molecular pathways controlling the release of CTGF by dying vascular cells and stressed fibroblasts using cell and molecular biology strategies in association with evaluation of human kidney biopsy samples.
Programme
Operating Grant
Emplacement
Quebec, Canada
Type de bénéficiaire
Not-for-profit organization or charity
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
253453
Name
Hébert Marie-Josée
Region
Québec
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Nutrition, Metabolism and Diabetes
Theme2
Biomedical
Prcname2
Hematology, Digestive Disease & Kidney
Projecttitle
Characterization of non-classical protein secretion pathways of importance in renal fibrosis triggered by the paracrine apoptotic program
Programtype2
Operating Grants
Orgnameinp2
Centre hospitalier de l'Université de Montréal (CHUM)
Cihramount2
$578,594
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Apoptosis; Autophagy; Caspases; Connective Tissue Growth Factor; Fibrosis; Nanovesicles; P53; Renal Failure; Transplantation; Vascular Rarefaction
Abstract
Injury to the vessels providing blood supply to the kidneys leads to abnormal renal healing, a leading cause of renal failure. We found that dying vascular cells release Connective Tissue Growth Factor (CTGF), a mediator implicated in abnormal healing. Fibroblasts, cells present within the kidney, also produce increased amounts of CTGF when stressed. Here we plan to characterize the genes and molecular pathways controlling the release of CTGF by dying vascular cells and stressed fibroblasts using cell and molecular biology strategies in association with evaluation of human kidney biopsy samples.
Competitiondate
201203
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Hébert, Marie-Josée
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $578,594~ $0~
