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• W2160410242 abstract "Abstract Zinc (Zn) deficiency during pregnancy results in a wide variety of developmental abnormalities. The objective of this study was to determine if expression of cardiac developmental genes regulated by Zn‐finger transcription factors could be modulated during dietary Zn deficiency. Rats were fed 0.5 (low Zn) or 90 (controls) µg Zn/g diet throughout pregnancy. Fetal development was examined and RNA isolated at gestation day (GD) 13 and 20. Cardiac abnormalities were detected at GD 20 in 82% of fetuses from dams fed low Zn diets compared with only 2% in controls. Cardiac developmental gene expression regulated by the Zn‐finger transcription factor, GATA‐4, was measured by quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR). In GD 13 and 20 hearts, two genes critical for heart development, α‐myosin heavy chain (α‐MHC) and cardiac troponin I (cTnI), were down‐regulated in Zn‐deficient fetuses. Expression of α‐MHC was 66 and 40% lower at GD 13 and 20, respectively, in fetuses from dams fed low Zn diets compared with fetuses from control dams ( p <0.05). Fetal cardiac TnI RNA levels were reduced 40 and 45% at GD 13 and 20 in the Zn‐deficient group compared with controls ( p <0.05). Fetal cardiac transcript levels of GATA‐4 and MHox, a gene regulated by a helix‐loop‐helix transcription factor, whose expressions are not Zn‐dependent, were unaffected by diet. These data indicated that alterations in gene regulation might be an underlying mechanism of cardiac abnormalities. Dysfunction of other Zn‐dependent transcription factors may be an integral part of the extensive teratogenesis associated with Zn deficiency. Birth Defects Res B 71:102–109, 2004. © 2004 Wiley‐Liss, Inc." @default.
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• W2160410242 date "2004-04-01" @default.
• W2160410242 modified "2023-10-14" @default.
• W2160410242 title "Cardiac abnormalities induced by zinc deficiency are associated with alterations in the expression of genes regulated by the zinc-finger transcription factor GATA-4" @default.
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• W2160410242 doi "https://doi.org/10.1002/bdrb.20004" @default.
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