Placental ceruloplasmin homolog is regulated by iron  and copper and is implicated in iron metabolism

Danzeisen, Ruth; Fosset, Cédric; Chariana, Zehane; Page, K.R.; David, Samuel; McArdle, Harry J

doi:10.1152/ajpcell.00019.2001

Cited by 43 publications

(44 citation statements)

References 33 publications

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“…This suggests that gestational copper deficiency, even when limited to the last two-thirds of gestation, limits iron transport to pups. This defective transfer of iron is consistent with limitation in a copper-dependent placental "ferroxidase" described previously (Danzeisen et al 2002).…”

Section: Discussionsupporting

confidence: 90%

Multiple mechanisms account for lower plasma iron in young copper deficient rats

Pyatskowit

Prohaska

2007

Biometals

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Copper deficiency lowers brain copper and iron during development. The reduced iron content could be due to hypoferremia. Experiments were conducted to evaluate plasma iron and "ferroxidase" hypotheses by determining copper and iron status of Holtzman albino rats following gestational/ lactational copper deficiency. Copper deficient (Cu−) dams on treatment for 5 weeks, two of gestation and three of lactation, had markedly lower copper content of milk and mammary tissue, and lower milk iron. Newborn pups from Cu− dams had lower copper and iron concentrations. Compared to Cu+ pups, Cu− pups, analyzed between postnatal age (P) 0 and P26, were smaller, anemic, had lower plasma iron, cardiac hypertrophy, and near zero ceruloplasmin activity. Liver copper in Cu+ pups increased then decreased during development and major reductions were evident in Cu− pups. Liver iron in Cu+ pups decreased with age while nursing but increased after eating solid food. Liver iron was lower in Cu− pups at P0 and P13 and normal at P20 and P26. Small intestinal copper decreased with age in Cu+ pups and was lower in Cu− pups. Intestinal iron levels in Cu-pups were higher than Cu+ pups postweaning in some experiments. Reduction in plasma iron in Cu− pups is likely due to a decreased "ferroxidase" function leading to lower placental iron transport, a lower milk iron diet, and partial block in iron uptake from intestine but is not due to failure to mobilize hepatic iron, in contrast to older rats eating diet with adequate iron.

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Section: Discussionsupporting

confidence: 90%

Multiple mechanisms account for lower plasma iron in young copper deficient rats

Pyatskowit

Prohaska

2007

Biometals

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“…In mammals, two multicopper ferroxidases, the plasma protein ceruloplasmin and its membrane-bound homologue haephestin, are involved in tissue iron mobilisation and cellular iron uptake (Mukhopadhyay et al, 1998;Vulpe et al, 1999). Further connections between the two metabolisms have been strengthened by the identification of a tissue specific GPI-anchored ceruloplasmin isoform identified in mammalian brain (Patel et al, 2000), as well as an haephestin-like ferroxidase in BeWo placental cell line (Danzeisen et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Identification of dietary copper- and iron-regulated genes in rat intestine

Marzullo

Tosco

Capone

et al. 2004

Gene

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“…It is likely that iron is exported as Fe(II) by iron-regulated protein 1 (IREG-1)/ferroportin-1 (FPN) (Abboud & Haile, 2000;Donovan et al, 2000;McKie et al, 2000) across the basolateral side of the STB. Transferrin has a higher affinity for Fe (III) compared to Fe(II); Danzeisen et al (2002) identified a copper oxidase in placental…”

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confidence: 99%