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Received January 21, 2004
Revised March 9, 2004
Accepted after revision May 4, 2004
1 University of Wyoming
2 New York University
* To whom correspondence should be addressed. E-mail: thansen{at}uwyo.edu.
Adequate maternal nutrient supply is critical for normal fetal organogenesis. We previously demonstrated that a global 50% nutrient restriction during the first half of gestation causes compensatory growth of both the left and right ventricles of the fetal heart by day 78 of gestation. Thus, it was hypothesized that maternal nutrient restriction significantly altered gene expression in the fetal cardiac left ventricle (LV). Pregnant ewes were randomly grouped into control (100% national research council [NRC] requirements) or nutrient-restricted groups (50% NRC requirements) from day 28 through day 78 of gestation, at which time fetal LV was collected. Fetal LV mRNA was used to construct a suppression subtraction cDNA library from which eleven cDNA clones were found by differential dot blot hybridization and virtual northern analysis to be up-regulated by maternal nutrient-restriction: caveolin, stathmin, G-1 cyclin, á-actin, titin, cardiac ankyrin repeat protein (CARP), cardiac-specific RNA-helicase activated by MEF2C (CHAMP), endothelial and smooth muscle derived neuropilin (ESDN), prostatic binding protein, NADH dehydrogenase subunit 2, and an unknown protein. Six of these clones (cardiac á-actin, cyclin G1, stathmin, NADH dehydrogenase subunit 2, titin, and prostatic binding protein) have been linked to cardiac hypertrophy in other species including humans. Of the remaining clones, caveolin, CARP, and CHAMP have been shown to inhibit remodeling of hypertrophic tissue. Compensatory growth of fetal LV in response to maternal under nutrition is concluded to be associated with increased transcription of genes related to cardiac hypertrophy, compensatory growth or remodeling. Counter-regulatory gene transcription may be increased, in part, as a response to moderating the degree of cardiac remodeling. The short and long-term consequences of these changes in fetal heart gene expression and induction of specific homeostatic mechanisms in response to maternal under nutrition remain to be determined.
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