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Transcriptional regulation of copper metabolism genes in the liver of fetal and neonatal control and iron-deficient rats.

Lenartowicz M, Kennedy C, Hayes H, McArdle HJ - Biometals (2014)

Bottom Line: Atp7b levels, in contrast, decreased from a maximum early in gestation to low levels in the term and post-natal livers.Ceruloplasmin expression appeared to be diametrically opposite to Atp7b.The other two metallochaperones showed the same pattern of expression as Atox1, with a decrease to term, a rise at Day 1, or a rise after birth followed by a brief decrease at about Day 3.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Gronostajowa 9, 30-387, Kraków, Poland.

ABSTRACT
Copper and iron metabolism have been known to interact for many years. We have previously shown, during pregnancy, that copper levels in the maternal liver rise as a consequence of iron deficiency, but that levels in the fetal liver decrease. In this paper, we measure expression of genes involved in copper metabolism in fetal and postnatal liver, to test whether alterations can explain this observation. Additionally, we study the extent to which gene expression changes in the latter stages of pregnancy and in the perinatal period. Ctr1 expression levels dropped to term, rising again thereafter. There was no difference in gene expression between control and iron deficient animals. Atox1 expression remained approximately stable until term, and then there was a rise to a maximum at about Day 8. Atp7a expression levels remained constant, except for a brief drop at term. Atp7b levels, in contrast, decreased from a maximum early in gestation to low levels in the term and post-natal livers. Ceruloplasmin expression appeared to be diametrically opposite to Atp7b. The other two metallochaperones showed the same pattern of expression as Atox1, with a decrease to term, a rise at Day 1, or a rise after birth followed by a brief decrease at about Day 3. None of the genes were significantly affected by iron deficiency, suggesting that changes in expression cannot explain the altered copper levels in the fetal and neonatal liver.

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Developmental changes in the expression level of the Ctr1 gene in the liver of the control and Fe deficient fetus and neonates. The mRNA level are shown relative to ubiquitin. Values with different letters differ significantly (p < 0.05). Data are expressed as mean ± SEM
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Fig2: Developmental changes in the expression level of the Ctr1 gene in the liver of the control and Fe deficient fetus and neonates. The mRNA level are shown relative to ubiquitin. Values with different letters differ significantly (p < 0.05). Data are expressed as mean ± SEM

Mentions: In the liver of both normal and iron deficient rats expression of the Ctr1 gene decreased from 17.5 to the 21.5 days gestation, then increased postnatally. There was no significant difference in expression between control and Fe deficient livers, though there was an apparent trend (p = 0.07) (Fig. 2). After entry to the hepatocytes, copper is bound to chaperone proteins. We measured mRNA levels of Atox1 in control and iron deficient fetal livers. There were no significant differences between the two groups at any stage of gestation or postnatal life (Fig. 3). As with Ctr1, levels decreased to term. After birth, levels rose in both control and Fe deficient pups. However, there was a decrease at Day 3. Currently, we do not have an explanation for this observation.Fig. 2


Transcriptional regulation of copper metabolism genes in the liver of fetal and neonatal control and iron-deficient rats.

Lenartowicz M, Kennedy C, Hayes H, McArdle HJ - Biometals (2014)

Developmental changes in the expression level of the Ctr1 gene in the liver of the control and Fe deficient fetus and neonates. The mRNA level are shown relative to ubiquitin. Values with different letters differ significantly (p < 0.05). Data are expressed as mean ± SEM
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4300417&req=5

Fig2: Developmental changes in the expression level of the Ctr1 gene in the liver of the control and Fe deficient fetus and neonates. The mRNA level are shown relative to ubiquitin. Values with different letters differ significantly (p < 0.05). Data are expressed as mean ± SEM
Mentions: In the liver of both normal and iron deficient rats expression of the Ctr1 gene decreased from 17.5 to the 21.5 days gestation, then increased postnatally. There was no significant difference in expression between control and Fe deficient livers, though there was an apparent trend (p = 0.07) (Fig. 2). After entry to the hepatocytes, copper is bound to chaperone proteins. We measured mRNA levels of Atox1 in control and iron deficient fetal livers. There were no significant differences between the two groups at any stage of gestation or postnatal life (Fig. 3). As with Ctr1, levels decreased to term. After birth, levels rose in both control and Fe deficient pups. However, there was a decrease at Day 3. Currently, we do not have an explanation for this observation.Fig. 2

Bottom Line: Atp7b levels, in contrast, decreased from a maximum early in gestation to low levels in the term and post-natal livers.Ceruloplasmin expression appeared to be diametrically opposite to Atp7b.The other two metallochaperones showed the same pattern of expression as Atox1, with a decrease to term, a rise at Day 1, or a rise after birth followed by a brief decrease at about Day 3.

View Article: PubMed Central - PubMed

Affiliation: Department of Genetics and Evolution, Institute of Zoology, Jagiellonian University, Gronostajowa 9, 30-387, Kraków, Poland.

ABSTRACT
Copper and iron metabolism have been known to interact for many years. We have previously shown, during pregnancy, that copper levels in the maternal liver rise as a consequence of iron deficiency, but that levels in the fetal liver decrease. In this paper, we measure expression of genes involved in copper metabolism in fetal and postnatal liver, to test whether alterations can explain this observation. Additionally, we study the extent to which gene expression changes in the latter stages of pregnancy and in the perinatal period. Ctr1 expression levels dropped to term, rising again thereafter. There was no difference in gene expression between control and iron deficient animals. Atox1 expression remained approximately stable until term, and then there was a rise to a maximum at about Day 8. Atp7a expression levels remained constant, except for a brief drop at term. Atp7b levels, in contrast, decreased from a maximum early in gestation to low levels in the term and post-natal livers. Ceruloplasmin expression appeared to be diametrically opposite to Atp7b. The other two metallochaperones showed the same pattern of expression as Atox1, with a decrease to term, a rise at Day 1, or a rise after birth followed by a brief decrease at about Day 3. None of the genes were significantly affected by iron deficiency, suggesting that changes in expression cannot explain the altered copper levels in the fetal and neonatal liver.

Show MeSH
Related in: MedlinePlus