The Intracellular Distribution of Ferritin Following Microinjection

Feldherr, Carl M.

doi:10.1083/jcb.12.1.159

Cited by 32 publications

(21 citation statements)

References 13 publications

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“…Furthermore, siRNA directed against the mRNA-encoding cytoplasmic human H-ferritin [28] decreases the presence of ferritin in SW1088 nuclei in a transient manner ( Figure 3A). Initial studies have suggested that cytoplasmic ferritin diffuses into the cell nucleus, although the data of Feldherr and co-workers [49,50] suggested that the mature 24-mer assembly may be too large to make the transit intact. The L-ferritin subunit was not detected in the nuclear fraction, consistent with previous publications on these cells from our laboratory [10] and also on other cell types by others [11,17,18].…”

Section: Discussionmentioning

confidence: 99%

Characterization of nuclear ferritin and mechanism of translocation

Surguladze

Patton

Cozzi

et al. 2005

Biochemical Journal

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Ferritin, normally considered a cytoplasmic iron-storage protein, is also found in cell nuclei. It is an established fact that H-ferritin is the major form of nuclear ferritin, but little is known about the roles of ferritin in nuclei or about the mechanisms that control its appearance within the nuclear volume. In the present study, we show that, for human SW1088 astrocytoma cells, the nuclear and cytoplasmic forms of H-ferritin are products of the same mRNA. Histochemical and biochemical evidence is presented showing that ferritin is distributed non-randomly within the nuclear volume and that it preferentially associates with heterochromatin. Both cytoplasmic and nuclear populations of H-ferritin contain mixtures of non- and O-glycosylated forms, but the nuclear population is enriched in O-glycosylated forms. Cells treated with alloxan, a potent inhibitor of O-glycosylation, contained significantly less nuclear ferritin compared with cells grown in control media. Alloxan inhibited the reappearance of H-ferritin in nuclei of cells released from conditions of iron depletion, but did not prevent its disappearance from nuclei of cells undergoing iron depletion. These results suggest that O-glycosylation accompanies the transfer of ferritin from the cytoplasm to the nucleus, but does not influence the reverse process. The picture that emerges is one in which ferritin translocation between the cytoplasm and the nucleus is post-translationally regulated and responds to environmental and nutritional cues.

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Section: Discussionmentioning

confidence: 99%

Characterization of nuclear ferritin and mechanism of translocation

Surguladze

Patton

Cozzi

et al. 2005

Biochemical Journal

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“…In an earlier study on Chaos chaos, it was found that ferritin can penetrate the nuclear membrane, the outer membrane of the mitochondrion, and the membrane lining the food vacuole, after it has been introduced into the ground cytoplasm by microinjection (1). Other work has shown that ferritin and methylated ferritin can be used to analyze the mechanism of pinocytosis in amebas and to follow some of the changes which take place within the cell during the digestion and assimilation of ingested materials (2).…”

Section: Introductionmentioning

confidence: 99%

THE USE OF COLLOIDAL GOLD FOR STUDIES OF INTRACELLULAR EXCHANGES IN THE AMEBA CHAOS CHAOS

Feldherr

Marshall

1962

The Journal of Cell Biology

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“…The VDAC pore is ≤3 nm in diameter, and this is the only gate between the cytoplasm and the mitochondrial intermembrane space [69]. In 1962, Feldherr showed that, after cell injection, ferritin was localized between the outer and inner mitochondrial membranes [70]. A similar distribution of ferritin could be seen in liver cells [71] and in skinned skeletal fibers [67].…”

Section: Nano-objects In Biomedical Researchmentioning

confidence: 92%

Delivery of nano-objects to functional Sub-domains of healthy and failing Cardiac myocytes

Lukyanenko

2007

Nanomedicine

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Cardiovascular disease, including heart failure, is one of the leading causes of mortality in the world. Delivery of nano-objects as carriers for markers, drugs or therapeutic genes to cellular organelles has the potential to sharply increase the efficiency of diagnostic and treatment protocols for heart failure. However, cardiac cells present special problems to the delivery of nano-objects, and the number of papers devoted to this important area is remarkably small. The present review discusses fundamental aspects, problems and perspectives in the delivery of nano-objects to functional sub-domains of failing cardiomyocytes. What size nano-objects can reach cellular sub-domains in failing hearts? What are the mechanisms for their permeation through the sarcolemma? How can we improve the delivery of nano-objects to the sub-domains? Answering these questions is fundamental to identifying cellular targets within the failing heart and the development of nanocarriers for heart-failure therapy at the cellular level.

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The Intracellular Distribution of Ferritin Following Microinjection

Cited by 32 publications

References 13 publications

Characterization of nuclear ferritin and mechanism of translocation

Characterization of nuclear ferritin and mechanism of translocation

THE USE OF COLLOIDAL GOLD FOR STUDIES OF INTRACELLULAR EXCHANGES IN THE AMEBA CHAOS CHAOS

Delivery of nano-objects to functional Sub-domains of healthy and failing Cardiac myocytes

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