The transferrin receptor: the cellular iron gate

Gammella, Elena; Buratti, Paolo; Cairo, Gaetano; Recalcati, Stefania

doi:10.1039/c7mt00143f

Cited by 213 publications

(181 citation statements)

References 84 publications

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“…Several proteins are involved in the synthesis of hemoglobin in red blood cells. TfR1 is the essential iron acquisition machinery of maturing erythroid cells (Kong, Gao & Chang, 2014;Gammella et al, 2017), while Mfrn1 and ALAS2 are required for heme biosynthesis (Hentze, Muckenthaler & Andrews, 2004;Amigo et al, 2011;Chiabrando, Mercurio & Tolosano, 2014). The expression of Mfrn1 and ALAS2 is transcriptionally regulated by transcription factor GATA-1 during erythroid maturation (Amigo et al, 2011;Tanimura et al, 2016).…”

Section: Agementioning

confidence: 99%

Iron homeostasis in a mouse model of thalassemia intermedia is altered between adolescence and adulthood

Sanyear

Butthep

Eamsaard

et al. 2020

PeerJ

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Background: Iron overload is one of common complications of β-thalassemia. Systemic iron homeostasis is regulated by iron-regulatory hormone, hepcidin, which inhibits intestinal iron absorption and iron recycling by reticuloendothelial system. In addition, body iron status and requirement can be altered with age. In adolescence, iron requirement is increased due to blood volume expansion and growth spurt. Heterozygous β-globin knockout mice (Hbb th3/+ ; BKO) is a mouse model of thalassemia widely used to study iron homeostasis under this pathological condition. However, effects of age on iron homeostasis, particularly the expression of genes involved in hemoglobin metabolism as well as erythroid regulators in the spleen, during adolescence have not been explored in this mouse model. Methods: Iron parameters as well as the mRNA expression of hepcidin and genes involved in iron transport and metabolism in wildtype (WT) and BKO mice during adolescence (6-7 weeks old) and adulthood (16-20 weeks old) were analyzed and compared by 2-way ANOVA. Results: The transition of adolescence to adulthood was associated with reductions in duodenal iron transporter mRNA expression and serum iron levels of both WT and BKO mice. Erythrocyte parameters in BKO mice remained abnormal in both age groups despite persistent induction of genes involved in hemoglobin metabolism in the spleen and progressively increased extramedullary erythropiesis. In BKO mice, adulthood was associated with increased liver hepcidin and ferroportin mRNA expression along with splenic erythroferrone mRNA suppression compared to adolescence. Conclusion: Our results demonstrate that iron homeostasis in a mouse model of thalassemia intermedia is altered between adolescence and adulthood. The present study underscores the importance of the age of thalassemic mice in the study of molecular or pathophysiological changes under thalassemic condition.Abboud S, Haile DJ. 2000. A novel mammalian iron-regulated protein involved in intracellular iron metabolism. AB, Paw BH. 2011. Identification of distal cis-regulatory elements at mouse mitoferrin loci using zebrafish transgenesis. Molecular and Cellular Biology 31 (7):

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Section: Agementioning

confidence: 99%

Iron homeostasis in a mouse model of thalassemia intermedia is altered between adolescence and adulthood

Sanyear

Butthep

Eamsaard

et al. 2020

PeerJ

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“…If indeed clathrin-coated vesicles fuse with the CCV during C. burnetii infection, the delivery of the cargo may be of upmost importance for replication and CCV expansion. Iron, for example, both is internalized by CME and is a requirement for C. burnetii growth, and it could serve as the necessary factor delivered by clathrin activity (230,231). However, iron acquisition is not likely to be the sole determinant in causing the drastic lack of replication in the absence of CHC, given that lysosomes which have recently undergone fusion with an autophagosome are already rich in iron (232)(233)(234).…”

Section: Coxiella Burnetiimentioning

confidence: 99%

Taming the Triskelion: Bacterial Manipulation of Clathrin

Latomanski

Newton

2019

Microbiol Mol Biol Rev

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SUMMARYThe entry of pathogens into nonphagocytic host cells has received much attention in the past three decades, revealing a vast array of strategies employed by bacteria and viruses. A method of internalization that has been extensively studied in the context of viral infections is the use of the clathrin-mediated pathway. More recently, a role for clathrin in the entry of some intracellular bacterial pathogens was discovered. Classically, clathrin-mediated endocytosis was thought to accommodate internalization only of particles smaller than 150 nm; however, this was challenged upon the discovery thatListeria monocytogenesrequires clathrin to enter eukaryotic cells. Now, with discoveries that clathrin is required during other stages of some bacterial infections, another paradigm shift is occurring. There is a more diverse impact of clathrin during infection than previously thought. Much of the recent data describing clathrin utilization in processes such as bacterial attachment, cell-to-cell spread and intracellular growth may be due to newly discovered divergent roles of clathrin in the cell. Not only does clathrin act to facilitate endocytosis from the plasma membrane, but it also participates in budding from endosomes and the Golgi apparatus and in mitosis. Here, the manipulation of clathrin processes by bacterial pathogens, including its traditional role during invasion and alternative ways in which clathrin supports bacterial infection, is discussed. Researching clathrin in the context of bacterial infections will reveal new insights that inform our understanding of host-pathogen interactions and allow researchers to fully appreciate the diverse roles of clathrin in the eukaryotic cell.

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“…La mayor proporción del RTf encontrado en el plasma es derivado de los glóbulos rojos y refleja la intensidad de la eritropoyesis y la demanda de hierro. También, la tasa circulante de receptor de la transferrina permite obtener una apreciación cuantitativa de la masa eritroblástica intramedular (32) . La concentración del RTf aumenta en la deficiencia de hierro y es un marcador de la severidad de la deficiencia de hierro.…”

Section: Receptor De Transferrinaunclassified

Biomarcadores del metabolismo y nutrición de hierro

Sermini¹,

Guerrero²,

Arredondo³

2017

Rev Peru Med Exp Salud Publica

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RESUMENLa anemia por deficiencia de hierro continúa siendo la deficiencia nutricional más abundante en el mundo, y son los lactantes, preescolares, mujeres en edad fértil y embarazadas los grupos de mayor susceptibilidad. Debido a esto es que se hace necesario el conocer los mecanismos de regulación de captación, transporte y absorción del metal a nivel celular, principalmente a nivel del enterocito y, una vez que el hierro entra a la circulación, conocer cuáles son los biomarcadores que permiten realizar un seguimiento del estatus del hierro corporal. En esta revisión mostramos, en primer lugar, cómo se regula la entrada de hierro a nivel de la célula del epitelio intestinal, mostrando las principales proteínas involucradas (transportadores de entrada y salida de hierro, oxido-reductasas, proteína de almacenamiento) y, para finalizar, hacemos un recuento de los principales biomarcadores del metabolismo de hierro una vez que este ha entrado y circula por el organismo. BIOMARKERS OF METABOLISM AND IRON NUTRITION ABSTRACTIron deficiency anemia is the most common nutritional deficiency worldwide, and the most susceptible groups are infants, preschoolers, women of childbearing age, and pregnant women. It is therefore essential to understand the mechanisms of regulation of iron uptake, transport, and absorption at the cellular level, particularly in enterocytes, and to identify blood biomarkers that allow the evaluation of iron status. This review describes how iron absorption is regulated by intestinal epithelial cells, the main proteins involved (iron transporters, oxidoreductases, storage proteins), and the main blood biomarkers of iron metabolism. INTRODUCCIÓN METABOLISMO DEL HIERROEl hierro es un mineral esencial para la vida debido a que participa en múltiples funciones enzimáticas involucradas tanto en el transporte de oxígeno, metabolismo energético y síntesis de ADN, entre otras (1) . El contenido normal de hierro en el organismo es de aproximadamente 4 g, de los cuales, 3 g forman parte de la hemoglobina, la mioglobina, las catalasas y otras enzimas respiratorias. El hierro almacenado corresponde a 0,5 g y, en su mayor parte, se encuentra depositado a nivel hepático (2) . A pesar de su gran importancia, el exceso de hierro se relaciona con morbilidad y mortalidad. Esto, debido a que puede producir daño celular por estrés oxidativo, mediante la generación de especies reactivas de oxigeno (ROS) a través de la reacción de Fenton, las cuales actúan sobre componentes biológicos como los lípidos, proteínas y ADN (3) , lo que determina que el metabolismo del hierro sea controlado por un potente sistema regulador. ABSORCIÓN DE FeEl hombre es capaz de reutilizar el hierro proveniente de la destrucción de los eritrocitos senescentes debido a la acción de los macrófagos del sistema retículo endotelial (4) . Además, del total de hierro que se moviliza diariamente, solo se pierde una pequeña proporción a través de las heces, orina, sudor y la descamación celular. Por lo que se requiere un pequeño aporte diario a travé...

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The transferrin receptor: the cellular iron gate

Cited by 213 publications

References 84 publications

Iron homeostasis in a mouse model of thalassemia intermedia is altered between adolescence and adulthood

Iron homeostasis in a mouse model of thalassemia intermedia is altered between adolescence and adulthood

Taming the Triskelion: Bacterial Manipulation of Clathrin

Biomarcadores del metabolismo y nutrición de hierro

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