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Query: UNIPROT:P02794 (ferritin)
 17,525 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mammalian ferritins can be resolved into multiple components by isoelectric focusing, and each tissue contains a characteristic subset of isoferritins. Ferritin isolated from human liver was compared to acidic ferritin isolated from mid-gestational human placenta to define a structural basis for ferritin heterogeneity. Placenta ferritin contained several major bands with isoelectric points in the range of pI = 4.7-5.0 which were more acidic than the predominant isoferritins of human liver. Ferritin from each tissue was resistant to denaturation by 10 M urea and appeared to be identical by electron microscopy. Circular dichroism measurements revealed that placenta ferritin had substantially less ordered secondary structure than liver ferritin. Both types of ferritin contained only two subunits when analyzed by electrophoresis in sodium dodecyl sulfate gels, but isoelectric focusing of dissociated subunits in urea revealed 6-7 different components. In this system, placenta ferritin was enriched in the more acidic subunits and it completely lacked the most basic subunits noted in liver ferritin; placental ferritin had no unique components. Differences in isoelectric points among assembled ferritins from these two tissues appear to result from different proportions of these acidic and basic subunits.
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PMID:Characterization of ferritin from human placenta. Implications for analysis of tissue specificity and microheterogeneity of ferritins. 53 48

Permeability of the continuous placental capillaries to macromolecules has been studied in the hemophagous region of the badger placenta by perfusion in situ of cationized ferritin (CF) in three phases of gestation (days 10 to 22, 22 to 30, and 30 to 40 after ovo-implantation). This ultrastructural tracer mapped luminal microdomains; such fixation on the luminal cell membrane was a preliminary step before its internalization into the cytoplasm. Lateral intercellular spaces (LIS) and vesicles were found to play an evolving role during gestation. Ultrastructural maturation of the capillary may be related to evolution of endothelial permeability. The LIS are involved in the transport of this macromolecule during the first two-thirds of pregnancy, and become progressively impermeable to the tracer as true, tight junctions are established between the adjacent endothelial cells. The enlargement of the vesicular population in luminal, cytoplasmic and abluminal positions and the increase in microfilaments could make vesicular transport more efficient in favouring cellular contractility. These ultrastructural findings that indicate that the optimal endothelial permeability to CF occurs during the second phase of pregnancy when the paraplacental hematoma reaches its maximal development and functional activity.
Placenta
PMID:Ultrastructural study of endothelial permeability to macromolecules in fetal paraplacental capillaries of European badger. 180 3

Trophoblast cells isolated from term human placenta and maintained as an adherent culture express surface receptors for transferrin as indicated by quantitative binding studies using 125I-labelled transferrin. The Kd was 5.3 x 10(-9) M. About 36 per cent of the total cell receptor population was found at the cell surface, the remainder being intracellular. Both 125I-labelled and 59Fe-labelled transferrin were internalized by receptor-mediated endocytosis with similar rates. Pulse-chase experiments showed that 125I-labelled transferrin was recycled and released back to the medium, whereas 59Fe accumulated intracellularly and was released slowly. Polyacrylamide gel electrophoresis followed by autoradiography revealed that 59Fe was accumulated by cells largely in the form of ferritin. A small intracellular pool of low molecular weight 59Fe was also detected. In the presence of monensin, the transfer of 59Fe to ferritin was greatly reduced. The nature and amount of 59Fe released from cells could be modulated by the incubation conditions. In the absence of chelating agents and iron salts, released 59Fe was found to be associated with a low molecular weight fraction as well as with transferrin and ferritin. The low molecular weight 59Fe readily formed a complex with added chelators such as apotransferrin, DTPA or desferrioxamine. The release of 59Fe could be increased by repeatedly changing the medium during the course of the incubation. 59Fe release from trophoblast cells exceeded the release of lactate dehydrogenase and also exceeded the release of 59Fe from 3T3 fibroblasts, suggesting a cell-specific process.
Placenta
PMID:Uptake and processing of 125I-labelled transferrin and 59Fe-labelled transferrin by isolated human trophoblast cells. 232 36

Receptor-mediated endocytosis is generally assumed to be the process by which the haemochorial placenta takes up iron from transferrin. The involvement of an additional nonendocytic process cannot, however, be excluded. It appears from a study of iron transport mechanisms and of the maturation of the transfer process that placental ferritin is involved in the transfer of iron from mother to fetus. The metabolic relationship between the ferritin pool and the placental transfer pool remains to be elucidated. There is no evidence for short-term regulation of placental transfer capacity in response to changes in the maternal iron supply or to changes in the trophoblastic iron content. This cannot yet be said of fetal feedback control of placental iron uptake because the experiments performed so far do not permit conclusions on this point. The capacity for iron uptake and transfer seems to increase in accordance with the ontogenetically determined placental growth pattern. This does not exclude long-range adaptive modifications of the transfer capacity in response to early maternal or fetal disturbances. The results obtained from studying placental maturation suggest that a possible long-term regulatory interaction between growing placenta and fetus may occur. Clinical evidence so far is inconclusive. The relatively moderate reductions in the fetal iron stores which are generally associated with severe iron-deficient pregnancies might be seen as an argument in favour of long-term placental control. The marked impact of pregnancy on maternal iron metabolism in rodents, as compared to other mammals, is possibly met by means of direct placental control of mucosal iron uptake. In primates, mucosal iron uptake during pregnancy seems to be governed by factors related to systemic iron deficiency only.
Placenta
PMID:Regulatory aspects of placental iron transfer--a comparative study. 304 6

Immunohistological studies on frozen sections of human placentae and breast carcinoma tissue using heteroantisera raised against both trophoblast microvillous plasma membrane preparations isolated from normal placentae and irradiated MCF-7 breast carcinoma cells have demonstrated a cell membrane antigen expressed by both normal human trophoblast and human breast carcinoma cells. The heteroantisera used in this study had all been previously adsorbed with immobilized human term pregnancy serum, placental alkaline phosphatase and placental ferritin preparations, as well as with human peripheral blood leucocytes. The oncoplacental membrane antigen would appear not to be represented in other normal tissues, but is represented on Jar choriocarcinoma cells and to a lesser degree on AV3 amniotic cells. Adsorption experiments have demonstrated that this antigen may not be dominant within the range of antigenic specificities of heteroantisera raised against MCF-7 cells or isolated trophoblast microvillous plasma membrane preparations.
Placenta
PMID:A cell membrane antigen expressed by both human breast carcinoma cells and normal human trophoblast. 616 65

Human amniotic epithelium has been found to consist of two cell types, known as dark and light cells, that are functionally different with respect to the passage of large molecules across the epithelium. Both cell types permit passage of ferritin intercellularly, whereas light cells incorporate this macromolecule. Dark cells impair the passage of 125I-PRL both inter- and intracellularly, whereas it is localized in light cells. In addition to a selectivity regarding the transmembrane passage of large molecules by the two cell types, we suggest that the osmoregulatory action of PRL on human amnion is restricted to the epithelial layer, and that its action may be mediated by light cells.
Placenta Suppl 1981
PMID:Differential responsiveness of cells of human amniotic epithelium to ferritin and 125I-prolactin in vitro. 696 65

The present study aims at the role of ferritin in the regulation of syncytiotrophoblast free iron levels. The differentiated cytotrophoblast cell in culture is used as a model for this maternal-fetal interface. Cytotrophoblast cells isolated from term placentae are cultured in iron-poor (Medium 199), iron-depleted [desferrioxamine(DFO)] and iron-supplemented [diferric transferrin (hTF-2Fe), ferric ammonium citrate (FAC)] medium. Distribution and de novo synthesis of isoferritins is studied, together with the cellular iron concentration and the ferritin iron saturation. Compared to ferritin isolated from total placenta, ferritin obtained from villous tissue is enriched with acidic isoforms. This observation is in agreement with measured light (L) to heavy (H) subunit ratios < 1 of de novo synthesized ferritin in cultured cytotrophoblast cells. Neither iron-poor culture medium, nor hTf-2Fe supplemented medium affects the cellular iron or ferritin concentration. FAC increased the cellular ferritin iron saturation and (by synthesis) the acidic isoferritin concentrations. The results strongly suggest, that the term syncytiotrophoblast is able to balance transferrin-mediated iron uptake and iron release. In case of FAC supplementation, the syncytiotrophoblast is unable to keep intracellular iron low, and ferritin synthesis is stimulated. The predominance of acidic ferritins and the preferential synthesis of H subunits can be functionally explained by the established fact that iron incorporation in acidic ferritins is faster due to the presence of ferroxidase centres. Damage by free iron catalysed hydroxyl radical formation is therefore minimized.
Placenta 1995 Jun
PMID:Ferritin in cultured human cytotrophoblasts: synthesis and subunit distribution. 756 1

Placental transferrin receptor (TfR) protein expression is increased in diabetic pregnancies that are complicated by low fetal iron stores, suggesting regulation of placental iron transport by fetoplacental iron status. In cell culture, iron homeostasis is regulated by coordinate stabilization of TfR mRNA and translation inactivation of ferritin mRNA by iron regulatory proteins (IRP-1 and -2) which bind to iron-responsive elements (IREs) on the respective mRNAs. Concentrations of IRP-1, IRP-2 and TfR mRNA were measured in 10 placentae obtained from diabetic and non-diabetic human pregnancies with a wide range of fetoplacental iron status. IRP-1 activity was present in human placenta and correlated closely with TfR mRNA concentration (r=0.82; P=0.007). IRP-2 activity and protein were not detected. In a second experiment, placentae were collected from 12 diabetic pregnancies, six with low fetal cord serum ferritin and placental non-heme iron concentrations, and six with normal iron status. IRP-1 activity and TfR Bmax for diferric transferrin were greater in the iron-deficient group (P<0.05). IRP-1 activity correlated inversely with cord serum ferritin (r=0.75; P<0.01) and placental non-heme iron (r=0.61; P=0.05) concentration. Placental IRP-1 activity is directly related to TfR mRNA concentration and is more highly expressed in iron-deficient placentae. The study provides direct in vivo evidence for IRP regulation of TfR expression in the human placenta.
Placenta 1999 Jan
PMID:Increased placental iron regulatory protein-1 expression in diabetic pregnancies complicated by fetal iron deficiency. 995 Jan 49

Human placental isoferritin (PLF) is a sub-type of human ferritin mainly composed of a 43 kD protein, which has an immunosuppressive activity and may be involved in the downregulation of the maternal immune system during pregnancy. The aim of this study was to evaluate the distribution of p43 in the placental tissue of abnormal first trimester pregnancies. Samples of villous and decidual tissues were collected between 7 and 12 weeks' gestation from 28 missed abortions and eight complete moles. Samples of placental tissue from 20 normal pregnancies of similar gestational age were used as controls. The localization of p43 was determined by immunohistochemical techniques using CM-H9 monoclonal antibody. Compared to controls, specific p43 immunoreactivity was low in the villous syncytiotrophoblast of missed abortions and absent from all villous cellular types in complete moles. These findings correlate well with the low level of maternal serum PLF found previously in early pregnancy failures and molar gestation. This suggests that PLF may be involved in the pathogenesis of early pregnancy disorders related to an abnormal placentation.
Placenta 2000 May
PMID:Diminished expression of placental isoferritin p43 component in first trimester abnormal pregnancies. 1083 77

Iron deficiency relatively often observed in pregnant women is assumed to be enhanced by cigarette smoking. The present studies are designed to determine the effect of maternal cigarette smoking during pregnancy on iron status of newborns. The levels of ferritin, as well as other iron-markers were determined in placenta tissue and in serum of umbilical cord blood. Placenta tissues and umbilical cord blood from healthy women (n = 30) were divided into smoking and non-smoking groups according to mothers plasma and urine cotinine levels. It is shown that total iron concentration in serum of umbilical cord was similar in both studied groups. In smoking group it was accompanied by higher total iron binding capacity which indicated that functional iron deficiency is possible. Iron storage ferritin in umbilical cord blood was 94 ng/ml and 163 ng/ml in smoking and non-smoking respectively. In placenta tissue mean level of ferritin was 252 micrograms/g in the smoking women whereas in the group of tobacco abstinent it was 320 micrograms/g. Low concentration of ferritin both in placenta and umbilical cord blood indicated that smoking during pregnancy could lead to subclinical iron deficiency in matched maternal-cord pairs.
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PMID:Effect of maternal smoking on some markers of iron status in umbilical cord blood. 1253 65


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