TRANSGENIC/KNOCKOUT ANIMALS IN MYOCARDIAL PRESERVATION
Project Number5R01HL056322-07
Contact PI/Project LeaderDAS, DIPAK K
Awardee OrganizationUNIVERSITY OF CONNECTICUT SCH OF MED/DNT
Description
Abstract Text
DESCRIPTION (adapted from abstract): This is a competing renewal application
for a grant funded for the past two years. In a continuing effort to develop an
appropriate molecular model to study the cellular defense of heart against
ischemic reperfusion injury, genetically engineered animals will be developed
and the molecular signaling process will be evaluated. Based on their recent
findings that oxygen free radicals function as second messengers in signal
transduction leading to phosphorylation and activation of heat shock protein
(HSP) 27, the investigators propose to develop transgenic and knockout mice for
HSP 27 and a related HSP--alpha, beta- crystallin. To test the importance of
redox signaling in myocardial ischemia/ reperfusion, mice genetically
engineered to affect two major proteins in redox regulation, thioredoxin and
glutaredoxin, will be developed. Since significant amounts of cross-talk exist
between heat shock and antioxidant proteins and since redox-sensing proteins
can regulate HSP, the investigators will study the underlying mechanisms by
examining the regulatory steps in intracellular signaling. Molecular signaling
will be correlated with standard measures of myocardial preservation, including
ventricular functions, cellular injury and infarction. Apoptosis and DNA
fragmentation as well as development of oxidative stress associated with
ischemic reperfusion injury will also be studied, as these parameters are
closely related to redox systems. Finally, the expression of the three
transcription factors AP-1, p53 and NFkB and the two protonocogenes c-jun and
c-fos will be examined, because these transcription factors and oncogenes are
believed to be the molecular links between ischemia/ reperfusion- induced
signal transduction and gene expression leading to the expression of heat shock
and antioxidant proteins. The results of these studies will demonstrate the
molecular mechanisms of constitutive cellular protection against myocardial
ischemia/ reperfusion injury by examining the redox signaling process.
Public Health Relevance Statement
Data not available.
NIH Spending Category
No NIH Spending Category available.
Project Terms
DNA damage antioxidants apoptosis cardiovascular disorder prevention cytotoxicity disease /disorder model free radical oxygen gene targeting genetic models genetically modified animals laboratory mouse model design /development myocardial ischemia /hypoxia myocardium oxidative stress protein structure function protooncogene reperfusion stress proteins thioredoxin transcription factor
No Sub Projects information available for 5R01HL056322-07
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