Ferritine

Résumé

La est une protéine permettant le stockage du fer. Elle joue un rôle clé dans le métabolisme du fer, permettant de réguler son absorption intestinale en fonction des besoins de l'organisme. Elle a ainsi une fonction de réserve et de détoxication du fer. Le dosage de la ferritine plasmatique est le reflet des réserves tissulaires mobilisables. Son dosage permet d'évaluer les réserves en fer et ainsi de dépister précocement une carence en fer ou à l'opposé d'apprécier une remontée des réserves lors d'un traitement par supplémentation ferrique. On la trouve dans le colostrum et la protéine de petit-lait, semble jouer des rôles biologiques très divers et est considérée comme la première ligne de défense immunitaire de l’organisme. Par sa très forte affinité avec le fer, elle favorise son absorption par la muqueuse intestinale des nouveau-nés. Elle a également des propriétés antibactériennes, antivirales, antifongiques, anti-inflammatoires, antioxydantes et immunomodulatrices. Les plan

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https://fr.wikipedia.org/wiki/Ferritine

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Le fer est l'élément chimique de numéro atomique 26, de symbole Fe. Le corps simple est le métal et le matériau ferromagnétique le plus courant dans la vie quotidienne, le plus souvent sous forme d

L'anémie, du grec (formé du privatif et du mot grec ancien , « sang »), est une anomalie de l'hémogramme caractérisée par une diminution du taux d'hémoglobine sous sa valeur normale. Ce manque ent

L'hémoglobine, couramment symbolisée Hb, parfois Hgb, est un pigment respiratoire (de la famille moléculaire des métalloprotéines, ici contenant du fer) présent essentiellement dans le sang des vert

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The course covers the regulation of gene expression, which translates the information contained in the genome into function, by adjusting the levels and activities of mRNAs and proteins to the needs of specific cells, tissues and environments. A particular emphasis is given on experimental methods.

Closely interfacing with bioengineering and medicine, this course provides foundational concepts in applying small-molecule chemical toolsets to probe the functions of living systems at the mechanistic and molecular level with emphasis placed on quantitative understanding and improving human health.

The labels "biosensor" and "eBiochip" have been employed to refer to the most diverse systems and in several fields of application. The course is meant not only to provide means to dig into this sea but also a thoughtful understanding of the detection principles and a design perspective.

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Disease tolerance is a defense strategy that limits the fitness costs of infection irrespectively of pathogen burden. While restricting iron (Fe) availability to pathogens is perceived as a host defense strategy, the resulting tissue Fe overload can be cytotoxic and promote tissue damage to exacerbate disease severity. Examining this interplay during malaria, the disease caused by Plasmodium infection, we find that expression of the Fe sequestering protein ferritin H chain (FtH) in mice, and ferritin in humans, is associated with reduced tissue damage irrespectively of pathogen burden. FtH protection relies on its ferroxidase activity, which prevents labile Fe from sustaining proapoptotic c-Jun N-terminal kinase (JNK) activation. FtH expression is inhibited by JNK activation, promoting tissue Fe overload, tissue damage, and malaria severity. Mimicking FtH's antioxidant effect or inhibiting JNK activation pharmacologically confers therapeutic tolerance to malaria in mice. Thus, FtH provides metabolic adaptation to tissue Fe overload, conferring tolerance to malaria.

Cell Press2012

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Iron is a transitional metal required by virtually all organisms as a dietary micromineral, indispensable for cellular survival and proliferation. The management of iron absorption and distribution in the organism and inside the cell must be tightly regulated in order to avoid the deleterious consequences of free iron-induced oxidative stress. Ferritin is the major protein responsible for iron storage and release of intracellular iron. Ferritin shells are formed from two types of subunits, known as H and L. The present work investigates the effects of conditional ferritin H deletion in mice. A broad ferritin H deletion in liver, spleen, bone marrow and thymus results in an alteration of iron metabolism, characterized by increased transferrin saturation and hepcidin mRNA levels and decreased liver iron deposits. Iron loading prior to deletion leads to liver failure early after deletion, showing that ferritin H is indispensable for limiting iron toxicity through iron sequestration. A hepatocyte-specific deletion fails to reproduce the same phenotype, suggesting an important role for Kupffer macrophages in liver iron detoxification. Ferritin H is also required for B lymphocyte survival, as indicated by the loss of mature B cells in an CD19-specific ferritin H deletion mouse strain, where this population is substantially reduced because of massive reactive oxygen species generation. Conditional deletion in heart leads to fibrosis, increased oxidative stress and to a switch towards a gene expression profile characteristic for cardiac hypertrophy, while iron loading prior to deletion causes a dramatic alteration of the cardiac output function and ultimately to heart failure. An intestine-specific ferritin H deletion results in a typical hemochromatotic phenotype, characterized by increased transferrin saturation and liver iron stores, increased hepcidin expression and decreased IRP2 activity. Hepcidin-mediated ferroportin downregulation at protein level is also shown not to be sufficient to limit the intestinal iron export. An modified version of the current model of intestinal iron absorption is proposed, that includes the function of ferritin H as an iron sink in intestine. This work contributes to a better understanding of iron metabolism in general and intestinal iron absorption in particular, and it might have an impact on the development of treatments against human hemochomatosis and anemia.

EPFL2009

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The objective was to explore how ferritin-H deletion influences Fe-59-distribution and excretion-kinetics in mice. Kinetics of Fe-59-release from organs, whole-body excretion, and distribution-kinetics of intravenously injected Fe-59 trace amounts were compared in iron-deficient and iron-replete mice with (Fth(Delta/Delta)) and without (Fth(lox/lox)) conditional Mx-Cre-induced ferritin-H deletion. Fe-59 was released from spleen and liver beginning on day 2 and day 5 after ferritin-H deletion, respectively, but was not excreted from the body. Plasma-Fe-59 was cleared significantly faster in iron-deficient Fth(Delta/Delta)-mice than in iron-adequate Fth(lox/lox)-controls. Fe-59-distribution showed a transient peak (e.g., in heart, kidney, muscle) in Fth(lox/lox) control mice, but not in ferritin-H deleted Fth(Delta/Delta) mice 24 hours after Fe-59 injection. Fe-59 uptake into the liver and spleen was significantly lower in iron-deficient Fth(Delta/Delta) than in Fth(lox/lox) mice 24 hours and 7 days after injection, respectively, and rapidly appeared in circulating erythrocytes instead. The rate of Fe-59 release after ferritin-H deletion supports earlier data on ferritin turnover in mammals; released Fe-59 is not excreted from the body. Instead, Fe-59 is channeled into erythropoiesis and circulating erythrocytes significantly more extensively and faster. Along with a lack of transient interim Fe-59 storage (e.g., in the heart and kidney), this finding is evidence for ferritin-related iron storage-capacity affecting rate and extent of iron utilization. (C) 2014 ISEH - Society for Hematology and Stem Cells. Published by Elsevier Inc.

Elsevier2014

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EPFL2009