Macrophage-HFE controls iron metabolism and immune responses in aged mice

Tangudu, Naveen K.; Yilmaz, Dilay; Wörle, Katharina; Gruber, Andreas; Colucci, Silvia; Leopold, Kerstin; Muckenthaler, Martina U.; Spasić, Maja Vujić

doi:10.3324/haematol.2019.235630

Cited by 7 publications

(13 citation statements)

References 15 publications

(23 reference statements)

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“…FPN could also play a role in HFE-linked genetic hemochromatosis. Recently, it has been shown that HFE deletion targeted to myeloid cells positively regulated FPN and prevented iron accumulation in macrophages of old mice [44]. These results, which confirm previous work indicating that iron export from macrophages is inhibited by HFE [45], are in line with the findings reported in a study preceding FPN identification and characterization, in which we found that macrophages of hemochromatosis patients were paradoxically iron deficient despite body iron overload [46].…”

Section: Lessons From Clinical Studies and Mouse Modelssupporting

confidence: 92%

Iron Availability in Tissue Microenvironment: The Key Role of Ferroportin

Gammella

Correnti

Cairo

et al. 2021

IJMS

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Body iron levels are regulated by hepcidin, a liver-derived peptide that exerts its function by controlling the presence of ferroportin (FPN), the sole cellular iron exporter, on the cell surface. Hepcidin binding leads to FPN internalization and degradation, thereby inhibiting iron release, in particular from iron-absorbing duodenal cells and macrophages involved in iron recycling. Disruption in this regulatory mechanism results in a variety of disorders associated with iron-deficiency or overload. In recent years, increasing evidence has emerged to indicate that, in addition to its role in systemic iron metabolism, FPN may play an important function in local iron control, such that its dysregulation may lead to tissue damage despite unaltered systemic iron homeostasis. In this review, we focus on recent discoveries to discuss the role of FPN-mediated iron export in the microenvironment under both physiological and pathological conditions.

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Section: Lessons From Clinical Studies and Mouse Modelssupporting

confidence: 92%

Iron Availability in Tissue Microenvironment: The Key Role of Ferroportin

Gammella

Correnti

Cairo

et al. 2021

IJMS

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“…This hypothesis has been investigated in mice with specific deletion of Hfe in myeloid‐derived cells, including liver resident macrophages (named Kupffer cells). The lack of HFE in Kupffer cells does not generate an hemochromatosis‐like phenotype but rather a mild iron deficiency at a very advanced age 6 . This demonstrates that there is no combinatorial effect of hepatocyte and macrophage HFE on hepcidin regulation.…”

Section: Figurementioning

confidence: 93%

“…The lack of HFE in Kupffer cells does not generate an hemochromatosis-like phenotype but rather a mild iron deficiency at a very advanced age. 6 This demonstrates that there is no combinatorial effect of hepatocyte and macrophage HFE on hepcidin regulation.…”

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confidence: 94%

Hfe Is Highly Expressed in Liver Sinusoidal Endothelial Cells But Is Not Needed to Maintain Systemic Iron Homeostasis In Vivo

et al. 2021

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“…19,20 Macrophages from HH patients and Hfe −/− mice have relatively low levels of iron, and this may exacerbate inflammatory responses. 36,37 Indeed, monocytes from HFE-HH patients produce lower levels of TNFα. 38 Additionally, the osteoclastic genes (Rank and Trap) were significantly decreased in the Hfe −/− mice, which was consistent with increased osteoclast numbers in trabecular bone.…”

Section: Discussionmentioning

confidence: 99%

Iron accumulation is associated with periodontal destruction in a mouse model of HFE‐related haemochromatosis

Han

Liu

Vaquette

et al. 2021

J of Periodontal Research

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Periodontitis is a destructive bacterial biofilm-induced chronic inflammatory disease. 1,2 Its hallmark is the destruction of the periodontium, including soft (periodontal ligament and gingiva) and hard (alveolar bone and cementum) tissues, potentially leading to tooth loss if not adequately treated in a timely manner. 3,4 Periodontal pathogens are associated with periodontitis development and progression. 5,6 Periodontitis is associated with an aberrant immune response to oral biofilms, with multiple risk factors contributing to its severity, including genetic predisposition, environmental factors (e.g., smoking) and systemic factors (e.g., diabetes), lifestyle and the oral microbiome. 7

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Macrophage-HFE controls iron metabolism and immune responses in aged mice

Cited by 7 publications

References 15 publications

Iron Availability in Tissue Microenvironment: The Key Role of Ferroportin

Iron Availability in Tissue Microenvironment: The Key Role of Ferroportin

Hfe Is Highly Expressed in Liver Sinusoidal Endothelial Cells But Is Not Needed to Maintain Systemic Iron Homeostasis In Vivo

Iron accumulation is associated with periodontal destruction in a mouse model of HFE‐related haemochromatosis

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