Maternal exercise reduces hyperthermia-induced apoptosis in developing mouse brain.

PURPOSE

Hyperthermia-induced apoptosis is mediated by mitochondrial pathway, and is temporally correlated with alterations in mitochondrial morphology in neuroepithelial cells. In addition, regular exercise up-regulates heat shock proteins (HSPs) that inhibit apoptosis. However, embryo-protective effects of maternal exercise against heat exposure during pregnancy have not been fully understood yet.

MATERIALS AND METHODS

To investigate the role of maternal exercise in protecting embryos from hyperthermia, we measured apoptosis-related factors and HSPs in Hsp70 knockout mouse embryos. Pregnant mice were divided into control, exercise, hyperthermia-after-exercise, and hyperthermia groups. Where appropriate the swimming exercise was performed for 5-10 min/day from embryonic day (ED) 1 to ED 8, and hyperthermia (43°C, 5 min) was induced on ED 8. To characterise the effects of maternal exercise on apoptosis-related factors and HSPs, we performed western blotting and transmission electron microscopy.

RESULTS

Caspase-9, -7, -3 and Bax were down-regulated in the hyperthermia-after-exercise group and Bcl-2, Hsp27 and Hsp110 were up-regulated. The number of apoptotic cells was markedly reduced in the hyperthermia-after-exercise group.

CONCLUSIONS

Maternal exercise plays an important role in inhibiting apoptotic cell death in embryos against hyperthermic exposure during pregnancy.