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A Murine Closed-chest Model of Myocardial Ischemia and Reperfusion
Published on: July 17, 2012
In vivo heat shock protects rat myocardial mitochondria
L Bornman1, C M Steinmann, G S Gericke
1Department of Chemistry and Biochemistry, Rand Afrikaans University, Johannesburg, South Africa.
Biochemical and Biophysical Research Communications
|June 10, 1998
Summary
Heat shock (HS) protects rat heart mitochondria from oxidative stress in vivo. This protection involves Hsp70 and heme oxygenase, preserving mitochondrial respiration.
Area of Science:
- Physiology
- Cell Biology
- Biochemistry
Background:
- Heat shock (HS) proteins (HSP) protect cells from various stresses, including oxidative stress.
- Mitochondria are known targets of HS-related protection in cultured cells.
Purpose of the Study:
- To investigate if mitochondria are also targets for HS-mediated protection in vivo.
- To determine the effect of HS on myocardial mitochondrial function in rats subjected to oxidative stress.
Main Methods:
- Sprague Dawley rats were exposed to heat shock (41°C, 15 min) or not.
- Hearts were excised after recovery and perfused with or without hydrogen peroxide (H2O2).
- Myocardial mitochondria were isolated and their oxygen consumption (state 3 respiration) was analyzed.
Main Results:
- HS prevented H2O2-induced alterations in state 3 mitochondrial respiration.
- HS increased the expression of heat shock protein 70 (Hsp70) and heme oxygenase (HO).
Conclusions:
- In vivo HS protects rat myocardial mitochondrial respiration against oxidative injury.
- This protection is associated with Hsp70 and/or HO expression and targets state 3 respiration.
