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Effects of maternal vitamin A status on fetal heart and lung: changes in expression of key developmental genes
C Antipatis1, C J Ashworth, G Grant
1Rowett Research Institute, Aberdeen AB21 9SB, United Kingdom.
Insights
Maternal vitamin A deficiency impaired fetal lung development in rats, reducing elastin and growth arrest-specific gene 6 (gas6) expression. These molecular changes highlight potential impacts on lung cell differentiation.
Area of Science:
- Developmental Biology
- Nutritional Science
- Molecular Biology
Background:
- Vitamin A is crucial for fetal development, particularly lung maturation.
- Elastin and growth arrest-specific gene 6 (gas6) are important structural and signaling molecules.
- Understanding nutrient-gene interactions is key to preventing developmental abnormalities.
Purpose of the Study:
- To investigate the impact of maternal vitamin A deficiency on fetal lung development in rats.
- To assess the expression of elastin and gas6 in fetal and neonatal lungs and hearts under vitamin A deficiency.
- To correlate morphological changes with molecular alterations in key genes.
Main Methods:
- Comparative study of normal-fed and vitamin A-deficient pregnant rats.
- Monitoring of fetal lung morphology and histology.
- Northern blotting to quantify elastin and gas6 mRNA levels in fetal and neonatal tissues (lung and heart).
Main Results:
- Vitamin A deficiency led to underdeveloped bronchial passageways and reduced elastic fiber staining in fetal lungs.
- Neonatal lungs showed reduced air space and smaller sacculi in deficient groups.
- Reduced mRNA levels of elastin and gas6 were observed in the fetal lung, with altered expression in the fetal and neonatal heart.
Conclusions:
- Maternal vitamin A deficiency significantly retards fetal lung development in rats.
- Altered expression of elastin and gas6 suggests impaired cell differentiation and structural integrity.
- These molecular markers may help identify affected cell types and developmental disruptions.
Abstract:
Vitamin A is required during pregnancy for fetal lung development. These experiments monitored fetal lung morphology in normal and vitamin A-deficient rats. The expression of elastin and the growth arrest-specific gene 6 (gas6) in fetal and neonatal hearts and lungs was assessed by Northern blotting. In normal-fed rats, elastin and gas6 were expressed in the fetal lung and heart from day 19 of gestation up to day 2 postnatally. Maternal vitamin A deficiency altered fetal lung development. On day 20, the bronchial passageways were less developed and showed reduced staining for elastic fibers, and in the neonates, the relative air space and the size of the sacculi were reduced. In the fetal lung, the mRNAs for elastin and gas6 were reduced to 56 and 68% of the control values, respectively. In the fetal heart, the mRNA for elastin was reduced to 64% of the control value, whereas gas6 was increased twofold. In the neonate, there was no change in elastin expression in the lung or heart, but gas6 expression in the heart was increased twofold. These results suggest that, in the pregnant rat, vitamin A deficiency may retard fetal lung development or influence the differentiation of critical cell lines. The changes in elastin and gas6 expression may be used to identify the cell types affected.