Grant: Operating Grant
University of Manitoba
$818,110.00
FGF2 Isoforms in Cardiac Hypertrophy
FY 2009-10
Summary
Many cardiovascular diseases are characterized by abnormal heart growth, which predicts poor cardiac outcome. Our previous studies have indicated that a protein, believed to be involved in promoting abnormal growth, FGF2, is more complex than generally known: FGF2 is made as both a 'long' version (Hi-FGF2) and a 'short' version (Lo-FGF2, and our data suggest that only the Hi-FGF2 version promotes hypertrophy (the 'bad' FGF) while the Lo-FGF2 version is actually beneficial. This poposal uses experimental mouse models of abnormal heart growth, as well as in vitro systems, to confirm and expand our data, and potentially provide a strategy that would convert the 'bad' FGF2 to its beneficial version (Lo FGF2). They may provide a means to prevent and even regress pathological hypertrophy.
Department
Program
Operating Grant
Recipient
Location
Manitoba, Canada
Recipient Type
Academia
Type
Grant
Source
CIHR Funding Decisions Database
As published
Id
189823
Name
Kardami Elissavet
Region
Manitoba
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Cardiovascular System - A: Cells and Tissues
Projecttitle
FGF2 Isoforms in Cardiac Hypertrophy
Programtype2
Operating Grants
Orgnameinp2
University of Manitoba
Cihramount2
$818,110
Cihrequipment2
$0
Programname2
Operating Grant
Keyworddelim
Cardiac Hypertrophy; Fibroblast-Myocyte Interaction; Fibrosis; Growth Factor Isoform; Signal Transduction; Transgenic Models
Abstract
Many cardiovascular diseases are characterized by abnormal heart growth, which predicts poor cardiac outcome. Our previous studies have indicated that a protein, believed to be involved in promoting abnormal growth, FGF2, is more complex than generally known: FGF2 is made as both a 'long' version (Hi-FGF2) and a 'short' version (Lo-FGF2, and our data suggest that only the Hi-FGF2 version promotes hypertrophy (the 'bad' FGF) while the Lo-FGF2 version is actually beneficial. This poposal uses experimental mouse models of abnormal heart growth, as well as in vitro systems, to confirm and expand our data, and potentially provide a strategy that would convert the 'bad' FGF2 to its beneficial version (Lo FGF2). They may provide a means to prevent and even regress pathological hypertrophy.
Competitiondate
200909
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Kardami, Elissavet
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $818,110~ $0~
