Regulation of transferrin receptor synthesis by human cytotrophoblast cells in culture

Kroos, M.J.; Starreveld, J. S.; Verrijt, C.E.H.; Eijk, H.G. Van; Dijk, J.P. van

doi:10.1016/0301-2115(95)02368-2

Cited by 16 publications

(6 citation statements)

References 12 publications

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“…35 In this study, we observed a significantly dose-responsive increase of TfR1 mRNA expression with DFO treatment and down-regulated expression with hTf-2Fe supplementation. It is consistent with the results from other studies 32,36 and suggests that the iron treatment in this study is effective.…”

Section: Discussionsupporting

confidence: 93%

Ferroportin 1 and hephaestin expression in BeWo cell line with different iron treatment

Bai

Cao

et al. 2011

Cell Biochemistry & Function

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The process of placental iron transfer is an important physiological process during pregnancy. However, the molecular mechanism of placental iron transport has not been completely elucidated until now. Ferroportin 1 (FPN1) and hephaestin (Heph) have been identified as the important molecules involved in duodenal iron export. However, whether they participate in the placental iron efflux has been undefined until now. In this study, the BeWo cells were treated with desferrioxamine and Holo-transferrin human in different concentrations and harvested at 48 and 72 h. The mRNA expression of FPN1 and Heph was detected with quantitative real-time polymerase chain reaction, and the protein expression was detected with western blots. The results showed an up-regulated FPN1 expression with desferrioxamine treatment and down-regulated expression with Holo-transferrin human supplementation. However, the change of FPN1 expression at protein level was limited. Heph expression enhanced when cells were treated with desferrioxamine although the quantity of Heph expression was low. Heph expression showed no significant change with Holo-transferrin human supplementation. It indicates that FPN1 may participate in placental iron transport, and placental FPN1 expression is obviously not dependent on the iron regular element/iron regular protein regulation. An alternatively spliced FPN1 isoform that lacks an iron regular element may be the predominant expression in BeWo cells. It also demonstrates that Heph is active in placenta but may not play a key role in placental iron transport because it is not the main part of placental copper oxidase.

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Section: Discussionsupporting

confidence: 93%

Ferroportin 1 and hephaestin expression in BeWo cell line with different iron treatment

Bai

Cao

et al. 2011

Cell Biochemistry & Function

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“…It is not clear what the functional effect this change in microvillous membrane TfR might have on iron transfer. TfR increases when iron is low and decreases when iron is high [30,31], independent of oxygen status. However, differences in maternal iron status are unlikely to explain our results, as maternal circulating transferrin concentrations were normal and equivalent at 1600 m versus 3100 m.…”

Section: Discussionmentioning

confidence: 98%

Effects of chronic hypoxia in vivo on the expression of human placental glucose transporters

2006

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Birth weight is reduced and the risk of preeclampsia is increased in human high altitude pregnancies. There has been little work to determine whether hypoxia acts directly to reduce fetal growth (e.g. reduced blood flow and oxygen delivery), or via changes in functional capacities such as nutrient transport. We therefore investigated the expression of a primary nutrient transporter, the GLUT1 glucose transporter and two in vitro markers of hypoxia (erythropoietin receptor, EPO-R, and transferrin receptor, TfR) in the syncytial microvillous (MVM) and basal membrane fractions (BMF) of 13 high (3100 m) and 12 low (1600 m) altitude placentas from normal term pregnancies. Birth weight was lower at 3100 m than at 1600 m despite similar gestational age, but none of the infants were clinically designated as fetal growth restriction. EPO-R, TfR and GLUT1 were examined by immunoblotting and maternal circulating erythropoietin and transferrin by ELISA. EPO-R was greater on the MVM (C75%) and BMF (C25%) at 3100 m. TfR was 32% lower on the MVM at 3100 m. GLUT1 was 40% lower in the BMF at 3100 m. Circulating EPO was greater at high altitude, while transferrin was similar, and neither correlated with their membrane receptors. BMF GLUT1 was positively correlated with birth weight at high, but not low altitude. In this in vivo model of chronic placental hypoxia, syncytial EPO-R increased as expected, while nutrient transporters decreased, opposite to what has been observed in vitro. Therefore, hypoxia acts to reduce fetal growth not simply by reducing oxygen delivery, but also by decreasing the density of nutrient transporters.

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“…It is noteworthy that DFX did not decrease the total intracellular content of iron compared with control cells, yet it resulted in an increase in TfR expression. Previous studies have found that cells increase their TfR synthesis when intracellular iron stores become depleted (Kroos et al . 1996; Tong et al .…”

Section: Discussionmentioning

confidence: 99%

Iron accumulation, iron‐mediated toxicity and altered levels of ferritin and transferrin receptor in cultured astrocytes during incubation with ferric ammonium citrate

Hoepken

Korten

Robinson

et al. 2004

Journal of Neurochemistry

126

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The cellular uptake and storage of iron have to be tightly regulated in order to provide iron for essential cellular functions while preventing the iron-catalysed generation of reactive oxygen species (ROS). In contrast to cells in other organs, little is known about the regulation of iron metabolism in brain cells, particularly in astrocytes. To investigate the regulation of iron metabolism in astrocytes we have used primary astrocyte cultures from the brains of newborn rats. After application of ferric ammonium citrate (FAC), cultured astrocytes accumulated iron in a time-(0-48 h) and concentration-dependent (0.01-1 mM) manner. This accumulation was prevented if FAC was applied in combination with the iron-chelator deferoxamine (DFX). Application of FAC to astrocyte cultures caused a strong increase in the cellular content of the iron storage protein ferritin and a decrease in the amount of transferrin receptor (TfR), which is involved in the transferrin-mediated uptake of iron into cells. In contrast, application of DFX strongly increased the level of TfR. Both up-regulation of ferritin content by iron application and up-regulation of TfR content by DFX were prevented by the protein synthesis inhibitor cycloheximide (CHX). During incubation of astrocytes with FAC, a mild and transient increase in the extracellular activity of the cytosolic enzyme lactate dehydrogenase and in the concentration of intracellular ROS was observed. In contrast, prevention of protein synthesis by CHX during incubation with FAC resulted in significantly more cell loss and a persistent and intense increase in the production of intracellular ROS. These results demonstrate that both iron accumulation and deprivation modulate the synthesis of ferritin and TfR in astrocytes and that protein synthesis is required to prevent iron-mediated toxicity in astrocytes.

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Regulation of transferrin receptor synthesis by human cytotrophoblast cells in culture

Cited by 16 publications

References 12 publications

Ferroportin 1 and hephaestin expression in BeWo cell line with different iron treatment

Ferroportin 1 and hephaestin expression in BeWo cell line with different iron treatment

Effects of chronic hypoxia in vivo on the expression of human placental glucose transporters

Iron accumulation, iron‐mediated toxicity and altered levels of ferritin and transferrin receptor in cultured astrocytes during incubation with ferric ammonium citrate

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