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Effect of maternal chronic hypoxic exposure during gestation on apoptosis in fetal rat heart

¹Center for Perinatal Biology, Department of Physiology and Pharmacology, and ²Department of Microbiology/Molecular Genetics, Loma Linda University School of Medicine, Loma Linda, California 92350

Submitted 3 January 2003 ; accepted in final form 13 May 2003

Chronic hypoxia during pregnancy is one of the most common insults to fetal development. We tested the hypothesis that maternal hypoxia induced apoptosis in the hearts of near-term fetal rats. Pregnant rats were divided into two groups, normoxic control and continuous hypoxic exposure (10.5% O₂) from day 15 to 21 of gestation. Hearts were isolated from fetal rats of 21-day gestational age. Maternal hypoxia increased hypoxia-inducible factor-1 protein in fetal hearts. Chronic hypoxia significantly increased the percentage and size of binucleated myocytes and increased apoptotic cells from 1.4 ± 0.14% to 2.7 ± 0.3% in the fetal heart. In addition, the active cleaved form of caspase 3 was significantly increased in the hypoxic heart, which was associated with an increase in caspase 3 activity. There was a significant increase in Fas protein levels in the hypoxic heart. Chronic hypoxia did not change Bax protein levels but significantly decreased Bcl-2 proteins. In addition, chronic hypoxia significantly suppressed expression of heat shock protein 70. However, chronic hypoxia significantly increased expression of the anti-apoptotic protein 14–3-3 , among other 14–3-3 isoforms. Chronic hypoxia differentially regulated -adrenoreceptor (-AR) subtypes with an increase in ₁-AR levels but no changes in ₂-AR. The results demonstrate that maternal hypoxia increases apoptosis in fetal rat heart, which may be mediated by an increase in Fas and a decrease in Bcl-2 proteins. Chronic hypoxia-mediated increase in ₁-AR and decrease in heat shock proteins may also play an important role in apoptosis in the fetal heart.

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