Cy. Su et al., CONSTITUTIVE AND INDUCIBLE HSP70S ARE INVOLVED IN OXIDATIVE RESISTANCE EVOKED BY HEAT-SHOCK OR ETHANOL, Journal of Molecular and Cellular Cardiology, 30(3), 1998, pp. 587-598
Improved cardiac post-ischemic recovery after whole-body hyperthermia
is correlated with an increased expression of the heat shock proteins
(hsps). The inducible hsp70 (hsp70i) has a known cardioprotective effe
ct against ischemia/reperfusion injury. Here, we studied whether other
hsps are also involved in cardioprotection. Using rat heart-derived H
9c2 myocytes, we observed that preheating at 43 degrees C for 20 min c
onferred resistance to hydrogen peroxide (H2O2). The resistance to mil
d H2O2 toxicity (3-5 mu mol/10(7) cells) appeared early and persisted,
whereas the resistance to moderate H2O2 toxicity (6-9 mu mol/10(7) ce
lls) was detectable only at 20-44 h post heat shock. No resistance was
observed at higher doses of hydrogen peroxide (10-12 mu mol/10(7) cel
ls), indicating that severe toxicity exceeds the capacity of the induc
ed protective mechanism. Coincidentally, this thermal regimen elicited
a rapid and prolonged increase in the cellular level of hsp70i, and a
delayed and transient induction of the constitutive hsp70 (hsp70c). N
uclear translocations of hsp70i and hsp70c also occurred upon heat sti
mulation. A homogeneous distribution of the accumulated hsp70i and hsp
70c throughout the nuclei and cytoplasm paralleled the development of
heat-induced resistance to moderate H2O2 challenge. Application of ano
ther hsp inducer, ethyl alcohol, evoked a similar pattern of H2O2 resi
stance, and hsp induction and distribution. Our results suggest that i
nduction and subcellular distribution of hsp70s contribute importantly
to cellular antioxidant defenses, and that a co-operation between hsp
70i and hsp70c may improve cardiac preservation during oxidative insul
t. (C) 1998 Academic Press Limited.