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Am J Physiol Heart Circ Physiol (May 15, 2003). doi:10.1152/ajpheart.00005.2003
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Submitted on January 3, 2003
Accepted on May 13, 2003

Effect of Maternal Chronic Hypoxic Exposure during Gestation on Apoptosis in Fetal Rat Heart

Soochan Bae1, Yuhui Xiao1, Guohu Li1, Carlos A Casiano2, and Lubo Zhang1*

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

* To whom correspondence should be addressed. E-mail: lzhang{at}som.llu.edu.

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{alpha} 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 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 HSP70. However, chronic hypoxia significantly increased expression of the anti-apoptotic protein 14-3-3 {theta}, among other 14-3-3 isoforms. Chronic hypoxia differentially regulated {beta}AR subtypes with an increase in {beta}1AR levels, but no changes in {beta}2AR. 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 hypoxic-mediated increase in {beta}1AR and decrease in heat shock proteins may also play an important role in apoptosis in the fetal heart.




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