The long term goal of this work is to provide a clearer understanding of the regulation and function of specific stress proteins in the ischemic heart. The overall hypothesis of the proposed work is that member(s) of the family of heat shock transcription factors exert complementary roles to activate stress proteins which attenuate cellular damage to the myocardium during ischemia and reperfusion. To test this hypothesis, we propose the following three specific aims: 1) To determine in vivo the precise temporal and spatial patterns of Hsp7o and Hsc70 mRNA expression within specific myocardial cells after bona fide myocardial ischemia. 2) To create mice deficient for heat shock transcriptional factors, mHSF1 and mHSF2, by gene-targeting in murine embryonic stem (ES) cells. 3) To elucidate more precisely the biological and functional role(s) of each specific HSF (aim2) during ischemia in transgenic mice.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Minority School Faculty Development Awards (K14)
Project #
1K14HL003155-01
Application #
2211233
Study Section
Special Emphasis Panel (ZHL1-CCT-L (F1))
Project Start
1994-05-01
Project End
1999-04-30
Budget Start
1994-05-01
Budget End
1995-04-30
Support Year
1
Fiscal Year
1994
Total Cost
Indirect Cost
Name
University of Texas Sw Medical Center Dallas
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
City
Dallas
State
TX
Country
United States
Zip Code
75390