Immune cells and hepatocytes express glycosylphosphatidylinositol-anchored ceruloplasmin at their cell surface

Marques, Liliana; Auriac, A; Willemetz, Alexandra; Banha, João; Silva, Bruno; Canonne‐Hergaux, François; Costa, Luciana

doi:10.1016/j.bcmd.2011.11.005

Cited by 61 publications

(54 citation statements)

References 53 publications

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“…Both Cp and APP proteins have been suggested to be involved in cellular Fe efflux through interaction with Fpn [23,24,[46][47][48]. Therefore, the present findings further corroborate our hypothesis of impairment on cellular Fe export as a key mechanism underlying AD pathogenesis.…”

Section: Discussionsupporting

confidence: 93%

“…In this context, our findings provide support for a role of impaired Fe metabolism in AD, through a change in Cp function as a partner of Fpn in the cellular Fe export axis. In fact, previous results from our group not only showed that human PBMCs constitutively express both soluble and membrane-anchored Cp isoforms [48,54], but also that GPI-Cp partially co-localizes with Fpn in lipid rafts of Fe-treated macrophages, where it could facilitate Fe export [48]. Moreover, this GPI-Cp/Fpn partial co-localization may indicate that besides GPI-Cp isoform, other proteins such as APP could be also involved in this process, as recently shown in neurons [23].…”

Section: Discussionmentioning

confidence: 87%

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Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients

Guerreiro

Silva

Crespo

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Alzheimer's disease (AD) is a neurodegenerative disorder of still unknown etiology and the leading cause of dementia worldwide. Besides its main neuropathological hallmarks, a dysfunctional homeostasis of transition metals has been reported to play a pivotal role in the pathogenesis of this disease. Dysregulation of iron (Fe) metabolism in AD has been suggested, particularly at the level of cellular iron efflux. Herein, we intended to further clarify the molecular mechanisms underlying Fe homeostasis in AD. In order to achieve this goal, the expression of specific Fe metabolism-related genes directly involved in Fe regulation and export was assessed in peripheral blood mononuclear cells (PBMCs) from 73AD patients and 74 controls by quantitative PCR. The results obtained showed a significant decrease in the expression of aconitase 1 (ACO1; P=0.007); ceruloplasmin (CP; P<0.001) and amyloid-beta precursor protein (APP; P=0.006) genes in AD patients compared with healthy volunteers. These observations point out to a significant downregulation in the expression of genes associated with ferroportin-mediated cellular Fe export in PBMCs from AD patients, when compared to controls. Taken together, these findings support previous studies suggesting impairment of Fe homeostasis in AD, which may lead to cellular Fe retention and oxidative stress, a typical feature of this disease.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 87%

Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients

Guerreiro

Silva

Crespo

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…HepG2 cells were used as a negative control for Fpn antibody specificity in our immunoblots. HepG2 cells express minimal Fpn (26). As a negative control for Hp antibody, C6 glioma cells were used (Fig.…”

Section: Resultsmentioning

confidence: 99%

Ferroportin and Exocytoplasmic Ferroxidase Activity Are Required for Brain Microvascular Endothelial Cell Iron Efflux

McCarthy

Kosman

2013

Journal of Biological Chemistry

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Background: Cellular iron efflux occurs via cooperation of ferroportin and a ferroxidase. Results: Depletion of ferroxidase and ferroportin from human brain microvascular endothelial cells decreases their ability to efflux iron. Conclusion: Iron efflux from brain microvascular endothelial cell ferroportin requires exocytoplasmic ferroxidase activity. Significance: The mechanism of iron efflux from endothelial cells of the blood-brain barrier is fundamental to how iron enters the brain.

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“…Ceruloplasmin (CP) plays an important role in iron metabolism as a ferroxidase, that facilitates cellular iron export by oxidizing Fe 2þ to Fe 3þ for incorporation into the extracellular iron transporter [2]. CP exists in a free secreted form in serum, and in a glycosylphosphatidylinositol (GPI)-anchored form in astrocytes [3], immune cells and hepatocytes [4]. Recent studies have indicate that CP is involved in the pathogenesis of PD [5].…”

Section: Introductionmentioning

confidence: 99%

Serum microRNA-133b is associated with low ceruloplasmin levels in Parkinson's disease

Zhao

Jin

Fei

et al. 2014

Parkinsonism & Related Disorders

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Immune cells and hepatocytes express glycosylphosphatidylinositol-anchored ceruloplasmin at their cell surface

Cited by 61 publications

References 53 publications

Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients

Decrease in APP and CP mRNA expression supports impairment of iron export in Alzheimer's disease patients

Ferroportin and Exocytoplasmic Ferroxidase Activity Are Required for Brain Microvascular Endothelial Cell Iron Efflux

Serum microRNA-133b is associated with low ceruloplasmin levels in Parkinson's disease

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