Analysis of the biologic functions of H- and L-ferritins in HeLa cells by transfection with siRNAs and cDNAs: evidence for a proliferative role of L-ferritin

Cozzi, Anna; Corsi, Barbara; Levi, Sonia; Santambrogio, Paolo; Biasiotto, Giorgio; Arosio, Paolo

doi:10.1182/blood-2003-06-1842

Cited by 113 publications

(102 citation statements)

References 42 publications

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“…because a recent study reported by Cozzi et. al., showed that ferritin H knockdown increased ferritin L expression in HeLa cells [9]. In this study the increased ferritin L expression did not affect iron availability [9].…”

Section: Discussionsupporting

confidence: 43%

“…al., showed that ferritin H knockdown increased ferritin L expression in HeLa cells [9]. In this study the increased ferritin L expression did not affect iron availability [9]. These results suggest that alterations in ferritin H expression may directly contribute to the altered iron metabolism and increased oxidative stress present during the disease progression of PD.…”

Section: Discussionmentioning

confidence: 43%

“…Overexpression of ferritin H in cells reduced free iron levels and increased cellular resistance to H 2 O 2 toxicity [27,28]. Deficiencies in ferritin lead to cellular profiles of oxidative stress and iron accumulation [9].…”

Section: Discussionmentioning

confidence: 99%

“…The heavy, or H, subunit is catalytically active, and induces oxidation of ferrous iron Fe(II) to ferric iron Fe(III) and aggregation of the oxidized iron inside the core, while the light (L) subunit does not have ferroxidase activity but may serve a structural function [2,8]. In this manner, ferritin functions to protect cells against iron-mediated toxicity [9,10]. Because of its important role, ferritin is tightly regulated at both the transcriptional and translational levels.…”

Section: Introductionmentioning

confidence: 99%

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Role and regulation of ferritin H in rotenone-mediated mitochondrial oxidative stress

Mackenzie

Ray

Tsuji

2008

Free Radical Biology and Medicine

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Tight regulation of intracellular iron levels in response to mitochondrial dysfunction is an important mechanism that prevents oxidative stress, thereby limiting cellular damage. Here, we describe a cytoprotective response involving transcriptional activation of the ferritin H gene in response to the mitochondrial complex I inhibitor and neurotoxic compound, rotenone. Rotenone exposure increased ferritin H mRNA and protein synthesis in NIH3T3 fibroblasts and SH-SY5Y neuroblastoma cells. Transient transfection of a ferritin H promoter-luciferase reporter into NIH3T3 cells showed that ferritin H was transcriptionally activated by rotenone through an antioxidant responsive element (ARE). Chromatin immunoprecipitation assays showed that rotenone treatment enhanced binding of Nrf2 and JunD transcription factors to the ARE. In addition, rotenone induced production of reactive oxygen species (ROS), and pretreatment with N-acetylcysteine abrogated ferritin H mRNA induction by rotenone, suggesting that this response is oxidative stress-mediated. Furthermore, reduced ferritin H expression by siRNA sensitized cells to rotenone-induced apoptosis with enhanced ROS production and annexin V positive cells. Taken together, these results suggest that ferritin H transcription is activated by rotenone via an oxidative stress-mediated pathway leading to ARE activation, and may be critically important to protect cells from mitochondrial dysfunction and oxidative stress.

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Section: Discussionsupporting

confidence: 43%

Section: Discussionmentioning

confidence: 43%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Role and regulation of ferritin H in rotenone-mediated mitochondrial oxidative stress

Mackenzie

Ray

Tsuji

2008

Free Radical Biology and Medicine

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“…It was shown that accumula- tion of ROS-generating substances (ATDR, iron-containing nanoparticles) by cells caused oxidation of these residues, formation of disulfide bonds and resulted in disturbances in protein conformation and interaction with mRNA causing increase of TFR1 expression [33]. Such phenomenon of sinchronous changes in FTH and TFR1 expression as a result of oxidative stress was observed by different groups of scientists on different cell lines [34,35].…”

Section: Discussionmentioning

confidence: 99%

Manifestation of Key Molecular Genetic Markers in Pharmacocorrection of Endogenous Iron Metabolism in MCF-7 and MCF-7/DDP Human Breast Cancer Cells

Чехун¹,

Lukianova²,

Demash³

et al. 2013

CellBio

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Effects of the nanocomposite and its components (magnetic fluid, cisplatin) on the level of endogenous iron exchange and the key links of genetic and epigenetic regulation of apoptotic program of sensitive and resistant MCF-7 cells were examined. We showed genetic and epigenetic mechanisms of action of nanocomposite of magnetic fluid and cisplatin. Nanocomposite caused elevation of number of cells in apoptosis in sensitive and especially resistant MCF-7 cells compared to cisplatin alone. It was proved that impact of nanocomposite on MCF-7/S and MCF-7/DDP cells caused more significant changes in expression of apoptosis regulators p53, Bcl-2 and Bax. We also suggested that changes in endogenous iron homeostasis and activation of free radical processes caused significant impact on apoptosis. Those changes included changes in methylation and expression of transferrin, its receptors, ferritin heavy and light chains (predominantly in resistant cell line), which caused activation of free radical synthesis and development of oxidative stress. We also showed that nanocomposite impact resulted into significant changes in expression of miRNA-34a and miRNA-200b, which regulated apoptosis, cell adhesion, invasion and activity of ferritin heavy chains gene. Thus, use of nanocomposite containing cisplatin and ferromagnetic as exogenous source of Fe ions caused changes of endogenous iron levels in sensitive and resistant cells allowing to increase specific activity of cytostatics and overcome factors, which promoted MDR development. Pharmacocorrection of endogenous iron metabolism allowed increasing antitumor activity of cisplatin and overcoming drug resistance.

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The Chemistry of Nature's Iron Biominerals in Ferritin Protein Nanocages

Theil¹,

Behera²

2013

Coordination Chemistry in Protein Cages

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Analysis of the biologic functions of H- and L-ferritins in HeLa cells by transfection with siRNAs and cDNAs: evidence for a proliferative role of L-ferritin

Abstract: The results indicate that L-ferritin has no direct effects on cellular iron homeostasis in HeLa cells, while it has new, ironunrelated functions. In addition, they suggest that H-ferritin function is to act as an iron

Cited by 113 publications

References 42 publications

Role and regulation of ferritin H in rotenone-mediated mitochondrial oxidative stress

Role and regulation of ferritin H in rotenone-mediated mitochondrial oxidative stress

Manifestation of Key Molecular Genetic Markers in Pharmacocorrection of Endogenous Iron Metabolism in MCF-7 and MCF-7/DDP Human Breast Cancer Cells

The Chemistry of Nature's Iron Biominerals in Ferritin Protein Nanocages

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