Uptake and distribution of transferrin and iron in perfused, iron-deficient rat liver

Holmes, J M; Morgan, Evan H.

doi:10.1152/ajpgi.1989.256.6.g1022

Cited by 3 publications

(4 citation statements)

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“…19 In ironloading diseases, the relative contribution of the lowaffinity process is likely to be even greater, 24,25 while under iron-deficient conditions the high-affinity process assumes greater significance. 26,27 The high-affinity uptake of Tf by hepatic cells, as in most cells, is mediated by Tf receptor 1 (TfR1). 28,29 TfR1 is a disulfide bonded homodimeric protein which traffics between the plasma membrane and various intracellular vesicular compartments.…”

Section: Tf-bound Ironmentioning

confidence: 99%

“…This explains why TfR1 levels are higher in the liver (and other tissues) in iron-deficient humans or experimental animals. 26,27,45,46 The opposite response is seen when cells have an excess of iron and a reduction in TfR1 expression serves to protect the cells from accumulating even more iron. Indeed, with heavy iron loading, such as that seen in patients with hemochromatosis or with secondary iron overload, TfR1 can be essentially undetectable in liver tissue.…”

Section: Tf-bound Ironmentioning

confidence: 99%

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Hepatic Iron Metabolism

2005

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The liver performs three main functions in iron homeostasis. It is the major site of iron storage, it regulates iron traffic into and around the body through its production of the peptide hepcidin, and it is the site of synthesis of major proteins of iron metabolism such as transferrin and ceruloplasmin. Most of the iron that enters the liver is derived from plasma transferrin under normal circumstances, and transferrin receptors 1 and 2 play important roles in this process. In pathological situations, non-transferrin-bound iron, ferritin, and hemoglobin/haptoglobin and heme/hemopexin complexes assume greater importance in iron delivery to the organ. Iron is stored in the liver as ferritin and, with heavy iron loading, as hemosiderin. The liver can divest itself of iron through the plasma membrane iron exporter ferroportin 1, a process that also requires ceruloplasmin. Hepcidin can regulate this iron release through its interaction with ferroportin.

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Section: Tf-bound Ironmentioning

confidence: 99%

Section: Tf-bound Ironmentioning

confidence: 99%

Hepatic Iron Metabolism

2005

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“…The number of transferrin receptors on the hepatocyte plasma membrane is relatively few [7], and at 37°C cellular uptake of iron continues to increase when the extracellular concentration of transferrin is increased far in excess of the concentration needed to saturate all transferrin receptors [34,48,50,51]. This has led some investigators to conclude that adsorptive or fluidphase endocytosis is the main mechanism of hepatocyte uptake of iron from transferrin [48,50,51].…”

Section: Thorstensen Unpublished Work)mentioning

confidence: 99%

“…This has led some investigators to conclude that adsorptive or fluidphase endocytosis is the main mechanism of hepatocyte uptake of iron from transferrin [48,50,51]. Such mechanisms would involve a receptor-independent release of iron from transferrin.…”

Section: Thorstensen Unpublished Work)mentioning

confidence: 99%

The role of transferrin in the mechanism of cellular iron uptake

Thorstensen

Romslo

1990

Biochemical Journal

187

106

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INTRODUCTIONThe role of transferrin and its cell surface receptor in cellular iron metabolism has received considerable interest during the last decade. Hence, over this period several reviews covering various aspects of the topic have been published.In this review we attempt to summarize the new knowledge and controversies encountered during the last 4-5 years. The focus is on iron metabolism by the hepatocyte. We also view the concept of transferrin-cell interactions from angles which previously may not have been given particular attention, and we include some aspects of iron metabolism not normally covered by reviews of this type. Central parts of what may be regarded as well-established knowledge either have been entirely omitted, or are only briefly described or mentioned to the extent considered relevant to the particular topic discussed. Important aspects of iron metabolism such as iron adsorption, haemochromatosis, ferritin iron and iron in infection and neoplasia are not covered in the present paper. Instead, the reader is referred to one or more of the recently published reviews [1-5] and references therein.

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Relationship between pinocytic rate and uptake of transferrin by suspended rat hepatocytes

Rudolph

Regoeczi

1991

Biol Metals

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The aim of this study was to compare quantitatively the capacity to transcytose (i.e. to uptake and release) transferrin (Tf) with the pinocytic activity of suspended adult rat hepatocytes. An oligodisperse preparation of 131I-polyvinylpyrrolidone (PVP; Mr 36,000) was used to measure the inward and outward aspects of the pinocytic process in separate experiments. Cell association of rat 125I-Tf was measured at Tf concentrations approaching physiological, where 59Fe uptake obeyed first-order kinetics. Release studies with both PVP and Tf were carried out under conditions which minimized the probability of de novo endocytosis of a molecule already released. Sets of experimental points representing cell-associated radioactivities were converted into continuous algebraic functions by fitting with two-term (release studies) or three-term (uptake studies) exponential equations. Transport of PVP and Tf through the cells was computed from these equations by deconvolution. This analysis showed that, under the present experimental conditions, the fractional transcytosis rates of Tf and PVP by hepatocytes were in the ratio of 1:0.77. These values imply that, in the physiological range of Tf concentrations, about 75% of the Fe taken up by hepatocytes may be due to a pinocytic mechanism (fluid-phase or mixed). Inclusion of chloroquine (1 mM) in the suspending medium, both in uptake and release experiments, resulted in more PVP and Tf passing through the cells, while Fe uptake was reduced. It is suggested that the base probably exerted its enhancing effect on transcytosis by shunting the subcellular transport of PVP and Tf to the outward leg through a shorter circuit.

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Uptake and distribution of transferrin and iron in perfused, iron-deficient rat liver

Cited by 3 publications

References 0 publications

Hepatic Iron Metabolism

Hepatic Iron Metabolism

The role of transferrin in the mechanism of cellular iron uptake

Relationship between pinocytic rate and uptake of transferrin by suspended rat hepatocytes

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