Maternal exercise reduces hyperthermia-induced apoptosis in developing mouse brain

Abstract

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.

• maternal hyperthermia, maternal exercise, apoptosis, heat shock proteins, Hsp70 knockout (KO) mouse embryos