Atherosclerosis

1998

DOI: 10.1016/s0021-9150(98)00033-1

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Colocalization of iron and ceroid in human atherosclerotic lesions

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Tzong‐Shyuan Lee

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et al.

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Discussion2

Mechanisms Of Lipofuscin Accumulation2

Iron Loading Promotes the Formation Of Oxidized Lipids Whic1

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Cited by 81 publications

(68 citation statements)

References 30 publications

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“…The characteristics of these cells in aged mouse ovaries were shared with foam cells, which are located in atherosclerotic foci. In foam cells, lipid peroxidation, ceroid accumulation, and autofluorescence have been observed (Lee et al 1998;Shashkin et al 2005;Levy et al 2007). Therefore, we identified the enlarged stromal cells in aged ovaries as macrophages with characteristics of foam cells.…”

Section: Discussionmentioning

confidence: 99%

“…This intracellular environment can promote oxidative stress in these cells, which was demonstrated by high MDA immunoreactivity. The contribution of the highly prooxidative environment in foam cells to the development of atherosclerotic lesions, with the co-localization of iron and ceroid, has been discussed (Lee et al 1998;Kockx et al 2003;Levy et al 2007). However, we did not observe significant oxidative effects in the tissue near the aggregations of enlarged macrophages, as there were no increased MDA immunostaining or degenerative changes.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Age-related Accumulation of Non-heme Ferric and Ferrous Iron in Mouse Ovarian Stroma Visualized by Sensitive Non-heme Iron Histochemistry

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2011

J Histochem Cytochem.

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SummarySensitive non-heme iron histochemistry-namely, the perfusion-Perls method and perfusion-Turnbull method-was applied to study the distribution and age-related accumulation of non-heme ferric iron and ferrous iron in mouse ovary. Light and electron microscopic studies revealed that non-heme ferric iron is distributed predominantly in stromal tissue, especially in macrophages. By contrast, the distribution of non-heme ferrous iron was restricted to a few ovoid macrophages. Aged ovaries exhibited remarkable non-heme iron accumulation in all stromal cells. In particular, non-heme ferrous iron level was increased in stromal tissue, suggestive of increased levels of redox-active iron, which can promote oxidative stress. Moreover, intense localization of both non-heme ferric and ferrous iron was observed in aggregated large stromal cells that were then characterized as ceroid-laden enlarged macrophages with frothy cytoplasm. Intraperitoneal iron overload in adult mice resulted in non-heme iron deposition in the entire stroma and generation of enlarged macrophages, suggesting that excessive iron accumulation induced macrophage morphological changes. The data indicated that non-heme iron accumulation in ovarian stromal tissue may be related to aging of the ovary due to increasing oxidative stress. (J Histochem Cytochem 60:229-242, 2012) Keywords non-heme iron, ovary, aging, macrophage, sensitive non-heme iron histochemistry Article

“…The characteristics of these cells in aged mouse ovaries were shared with foam cells, which are located in atherosclerotic foci. In foam cells, lipid peroxidation, ceroid accumulation, and autofluorescence have been observed (Lee et al 1998;Shashkin et al 2005;Levy et al 2007). Therefore, we identified the enlarged stromal cells in aged ovaries as macrophages with characteristics of foam cells.…”

Section: Discussionmentioning

confidence: 99%

“…This intracellular environment can promote oxidative stress in these cells, which was demonstrated by high MDA immunoreactivity. The contribution of the highly prooxidative environment in foam cells to the development of atherosclerotic lesions, with the co-localization of iron and ceroid, has been discussed (Lee et al 1998;Kockx et al 2003;Levy et al 2007). However, we did not observe significant oxidative effects in the tissue near the aggregations of enlarged macrophages, as there were no increased MDA immunostaining or degenerative changes.…”

Section: Discussionmentioning

confidence: 99%

Age-related Accumulation of Non-heme Ferric and Ferrous Iron in Mouse Ovarian Stroma Visualized by Sensitive Non-heme Iron Histochemistry

¹

2011

J Histochem Cytochem.

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SummarySensitive non-heme iron histochemistry-namely, the perfusion-Perls method and perfusion-Turnbull method-was applied to study the distribution and age-related accumulation of non-heme ferric iron and ferrous iron in mouse ovary. Light and electron microscopic studies revealed that non-heme ferric iron is distributed predominantly in stromal tissue, especially in macrophages. By contrast, the distribution of non-heme ferrous iron was restricted to a few ovoid macrophages. Aged ovaries exhibited remarkable non-heme iron accumulation in all stromal cells. In particular, non-heme ferrous iron level was increased in stromal tissue, suggestive of increased levels of redox-active iron, which can promote oxidative stress. Moreover, intense localization of both non-heme ferric and ferrous iron was observed in aggregated large stromal cells that were then characterized as ceroid-laden enlarged macrophages with frothy cytoplasm. Intraperitoneal iron overload in adult mice resulted in non-heme iron deposition in the entire stroma and generation of enlarged macrophages, suggesting that excessive iron accumulation induced macrophage morphological changes. The data indicated that non-heme iron accumulation in ovarian stromal tissue may be related to aging of the ovary due to increasing oxidative stress. (J Histochem Cytochem 60:229-242, 2012) Keywords non-heme iron, ovary, aging, macrophage, sensitive non-heme iron histochemistry Article

“…21 Figure 4B). In line, iron loading of M2 macrophages in vitro resulted in increased expression of the LXR target genes ABCA1, ABCG1, and apolipoprotein E ( Figure 4D-4F).…”

Section: Iron Loading Promotes the Formation Of Oxidized Lipids Whicmentioning

confidence: 95%

Liver X Receptor Activation Stimulates Iron Export in Human Alternative Macrophages

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et al. 2013

Circulation Research

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Rationale: In atherosclerotic plaques, iron preferentially accumulates in macrophages where it can exert pro-oxidant activities. Objective: The objective of this study was, first, to better characterize the iron distribution and metabolism in macrophage subpopulations in human atherosclerotic plaques and, second, to determine whether iron homeostasis is under the control of nuclear receptors, such as the liver X receptors (LXRs). Methods and Results: Here we report that iron depots accumulate in human atherosclerotic plaque areas enriched in CD68 and mannose receptor (MR)-positive (CD68 + MR + ) alternative M2 macrophages. In vitro IL-4 polarization of human monocytes into M2 macrophages also resulted in a gene expression profile and phenotype favoring iron accumulation. However, M2 macrophages on iron exposure acquire a phenotype favoring iron release, through a strong increase in ferroportin expression, illustrated by a more avid oxidation of extracellular low-density lipoprotein by iron-loaded M2 macrophages. In line, in human atherosclerotic plaques, CD68 + MR + macrophages accumulate oxidized lipids, which activate LXRα and LXRβ, resulting in the induction of ABCA1, ABCG1, and apolipoprotein E expression. Moreover, in iron-loaded M2 macrophages, LXR activation induces nuclear factor erythroid 2-like 2 expression, thereby increasing ferroportin expression, which, together with a decrease of hepcidin mRNA levels, promotes iron export. Conclusions: These data identify a role for M2 macrophages in iron handling, a process regulated by LXR activation.

“…In professional scavengers, such as RPE cells and macrophages (foam cells) in atheroma, a large portion of lipofuscin (or ceroid) originates from endocytosed material (Lee et al, 1998, Nilsson et al, 2003. Depending on the nature of the autophagocytosed/endocytosed material, the composition of lipofuscin varies amongst different types of postmitotic cells, and no chemical formula can be given for this complex substance that is mainly composed of cross-linked protein and lipidaceous material (Brunk and Terman, 2002).…”

Section: Lysosomal Accumulation Of Lipofuscin and Its Influence Omentioning

confidence: 99%

The role of lysosomes in iron metabolism and recycling

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2011

The International Journal of Biochemistry & Cell Biology

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Iron is the most abundant transition metal in the earths crust. It cycles easily between ferric (oxidized; Fe(III)) and ferrous (reduced; Fe(II)) and readily forms complexes with oxygen, making this metal a central player in respiration and related redox processes. However, loose iron, not within heme or iron-sulfur cluster proteins, can be destructively redox-active, causing damage to almost all cellular components, killing both cells and organisms. This may explain why iron is so carefully handled by aerobic organisms. Iron uptake from the environment is carefully limited and carried out by specialized iron transport mechanisms. One reason that iron uptake is tightly controlled is that most organisms and cells cannot efficiently excrete excess iron. When even small amounts of intracellular free iron occur, most of it is safely stored in a non-redox-active form in ferritins. Within nucleated cells, iron is constantly being recycled from aged iron-rich organelles such as mitochondria and used for construction of new organelles. Much of this recycling occurs within the lysosome, an acidic digestive organelle. Because of this, most lysosomes contain relatively large amounts of redox-active iron and are therefore unusually susceptible to oxidant-mediated destabilization or rupture. In many cell types, iron transit through the lysosomal compartment can be remarkably brisk. However, conditions adversely affecting lysosomal iron handling (or oxidant stress) can contribute to a variety of acute and chronic diseases. These considerations make normal and abnormal lysosomal handling of iron central to the understanding and, perhaps, therapy of a wide range of diseases

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