Expression of heat shock proteins in turtle and mammal hearts: relationship to anoxia tolerance

Heat shock proteins (HSPs) may play a cardioprotective role during hypoxia or ischemia. We hypothesized that cardiac tissue from hypoxia-tolerant animals might have high levels of specific HSPs. We measured myocardial HSP60 and HSP72/73 in painted and softshell turtles during normoxia and anoxia (12 h) and after recovery (12 or 24 h). We also measured myocardial HSPs in normoxic rats and rabbits. During normoxia, hearts from the most highly anoxia-tolerant species, the painted turtle, expressed the highest levels of HSP60 (22.6 +/- 2.0 mg/g total protein) followed by softshells (11.5 +/- 0.8 mg/g), rabbits (6.8 +/- 0.9 mg/g), and rats (4.5 +/- 0.5 mg/g). HSP72/73 levels, however, were not significantly different. HSP60 levels in hearts from both painted and softshell turtles did not deviate significantly from control values after either 12 h of anoxia or 12 or 24 h of recovery. The pattern of changes observed in HSP72/73 was quite different in the two turtle species. In painted turtles anoxia induced a significant increase in myocardial HSP72/73 (from 2.8 +/- 0.1 mg/g normoxic to 3.9 +/- 0.2 mg/g anoxic, P < 0.05). By 12 h of recovery, HSP72/73 had returned to control levels (2.7 +/- 0.1 mg/g) and remained there through 24 h (2.6 +/- 0.2 mg/g). In softshell turtles, HSP72/73 decreased significantly after 12 h of anoxia (from 2.4 +/- 0.4 mg/g normoxic to 1.3 +/- 0.2 mg/g anoxic, P < 0.05). HSP72/73 levels were still slightly below control after 12 h of recovery (2.1 +/- 0.1 mg/g) and then rose to significantly above control after 24 h of recovery (4.1 +/- 0.7 mg/g, P < 0.05). We also conclude that anoxia-tolerant and anoxia-sensitive turtles exhibit different patterns of myocardial HSP changes during anoxia and recovery. Whether these changes correlate with their relative degrees of anoxia tolerance remains to be determined.