Iron deprivation‐induced apoptosis in HL‐60 cells

Fukuchi, Kunihiko; Tomoyasu, Shigeru; Tsuruoka, Nanae; Gomi, Kunihide

doi:10.1016/0014-5793(94)00755-1

Cited by 86 publications

(58 citation statements)

References 6 publications

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“…Although it has been shown that DFB has a toxic effect on eukaryotic cells (Fukuchi et al 1994, Leardi et al 1998, we have demonstrated that this is not the case for our heterotrophic bioreporter (Fig. 5).…”

Section: Specificity Of Fe-siderophore Acquisition and Cross-utilizationcontrasting

confidence: 72%

Virus and siderophore-mediated transfer of available Fe between heterotrophic bacteria: characterization using an Fe-specific bioreporter

Mioni¹,

Poorvin²,

Wilhelm³

2005

Aquat. Microb. Ecol.

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Although marine chemists can accurately quantify both the concentration of dissolved iron (Fe) and the high-affinity organic ligands which complex Fe in surface waters, tools to characterize the relative bioavailability of such organically bound Fe complexes remain unavailable. In this study, we compared the bioavailability of Fe released from the lysis of the heterotrophic bacterium Vibrio natriegens PWH3a to that of Fe complexed to synthetic chelators (EDTA) and siderophores (including the trihydroxamate desferrioxamine B [DFB] and 2 catecholates isolated from Fe-limited heterotrophic bacterial cultures) using a heterotrophic bioluminescent reporter of Fe availability (Pseudomonas putida FeLux). Using the bioluminescent response of P. putida FeLux, we were able to rank the Fe sources tested here in a decreasing order of bioavailability: lysates > Fe-homologous catecholate (from a P. putida FeLux culture) ~ Fe-exogenous catecholate (from V. natriegens culture) > inorganic Fe (FeCl 3 , 15 nM) ~ Fe(III)' from EDTA-buffered treatment (pFe 18.12) > Fe:DFB, where pFe is -log [Fe 3+ ]. Combined with estimates of Fe assimilation of 55 Fe-labeled lysates, our data further demonstrate that organic Fe complexes released during virus-mediated cell lysis are ca. 1000 times more bioavailable and efficiently assimilated by bacterial cells than Fe(III)'. Our results validate the utilization of P. putida FeLux as a bioreporter of Fe-bioavailability and also support the assumption that virus activity plays a crucial role in the regeneration of biologically available Fe complexes in surface seawater. KEY WORDS: Iron availability · Bioreporter · Heterotrophic bacteria · Siderophore · Virus lysates Resale or republication not permitted without written consent of the publisherAquat Microb Ecol 41: [233][234][235][236][237][238][239][240][241][242][243][244][245] 2005 these organic ligands in natural systems, recent experiments suggest that the chemical nature of these Fe complexes may influence competition between prokaryotes and eukaryotes (Hutchins et al. 1999a, Poorvin et al. 2004.The similarities between the stability constants ( Lewis et al. 1995, Rue & Bruland 1995 and structural groups (Martinez et al. 2003, Gledhill et al. 2004) of the natural organic Fe ligands and those for naturally produced siderophores has led to a surge of interest in the microbial component of the marine plankton assemblage. It has been demonstrated that marine heterotrophic bacteria account for as much as 50% of the biomass (and thus biogenic Fe) in oceanic systems (Tortell et al. 1999). Furthermore, bacteria contain significantly more Fe per biomass unit than phytoplankton and are responsible for significant Fe uptake in Fe-depleted seawaters (Tortell et al. 1996). In addition, although several studies have shown that bacterial productivity was co-limited by carbon and Fe (Church et al. 2000, Kirchman et al. 2000, other studies suggest that heterotrophic bacterial productivity may be directly Fe-limited at low, in situ concentra...

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Section: Specificity Of Fe-siderophore Acquisition and Cross-utilizationcontrasting

confidence: 72%

Virus and siderophore-mediated transfer of available Fe between heterotrophic bacteria: characterization using an Fe-specific bioreporter

Mioni¹,

Poorvin²,

Wilhelm³

2005

Aquat. Microb. Ecol.

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“…For example, iron chelation has been demonstrated to induce apoptosis (Fukuchi et al, 1994;Haq et al, 1995) and promote cell-cycle arrest (Lederman et al, 1984). Similarly, cellular hypoxia represents a potent stimulus for the apoptotic cascade (for a review, see Brunelle and Chandel, 2002).…”

Section: Discussionmentioning

confidence: 99%

Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

et al. 2004

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Regulatory interferences at the iron transporter ferroportin 1 (Fpn1) cause transient defects in iron homeostasis and erythropoiesis in polycythaemia(Pcm) mutant mice. The present study identified decreased Fpn1 expression in placental syncytiotrophoblast cells at late gestation as the mechanism of neonatal iron deficiency in Pcm mutants. Tissue specificity of embryonic Fpn1 dysregulation was evident from concomitant decreases in Fpn1 mRNA and protein expression in placenta and liver, as opposed to upregulation of Fpn1 protein despite decreased transcript levels in spleen, implicating post-transcriptional regulation of Fpn1. Dysregulation of Fpn1 and decreased iron levels in Pcm mutant spleens correlated with apoptotic cell death in the stroma, resulting in a semidominant spleen regression. At 7 weeks of age, a transient increase in spleen size in Pcm heterozygotes reflected a transient erythropoietin-mediated polycythemia. Structurally, Pcm mutant spleens displayed a severe defect in red pulp formation, including disruption of the sinusoidal endothelium, as well as discrete defects in white pulp organization during postnatal development. Reduced functional competence of the Pcmmutant spleen was manifested by an impaired response to chemically induced hemolytic anemia. Thus, aberrant Fpn1 regulation and iron homeostasis interferes with development of the spleen stroma during embryogenesis,resulting in a novel defect in spleen architecture postnatally.

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“…DFO, that mimics hypoxia and a similar oxygen sensor in the hypoxia regulation, induces a hypoxic condition (Tazuke et al, 1998;Park et al, 2000;Park et al, 2001a). The effect of DFO on DNA synthesis and repair was reflected in studies that have shown that treatment with DFO induces apoptosis in rapidly growing tumor cells (Fukuchi et al, 1994;Simonart et al, 2000). This new finding indicates that there is another pathway that is different from the HIF-1 signaling pathway, which is known as a major mechanism in hypoxia signaling.…”

Section: Introductionmentioning

confidence: 96%

Hypoxia activates the cyclin D1 promoter via the Jak2/STAT5b pathway in breast cancer cells

Joung

Lim²,

Lee³

et al. 2005

Exp Mol Med

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Hypoxia, a common consequence of solid tumor growth in breast cancer or other cancers, serves to propagate a cascade of molecular pathways which include angiogenesis, glycolysis, and various cellcycle control proteins. As we have shown previously, hypoxia activates STAT5 (signal transducer and activator of transcription 5) and increases its binding activity to the GAS element in mammary epithelial cells. In this study we attempted to elucidate the mechanism by which cyclin D1 is regulated by the STAT5 protein under hypoxic conditions. Our data demonstrate that hypoxia (2% O 2 ) or desferrioxamine (DFO) induces tyrosine and serine phosphorylation of STAT5 in human breast cancer cells (MCF-7) and mammary epithelial cells (HC11). Imunoprecipitation and subsequent Western analysis showed that Jak2 leads to the tyrosine phosphorylation and activation of STAT5a or STAT5b under hypoxic conditions. Using a transfected COS-7 cell model system, we demonstrate that the activity of a cyclin D1 promoter-luciferase construct increased under hypoxic conditions or DFO treatment. The activity of the STAT5b/cyclin D1 promoter increased significantly by 12 h of hypoxia, whereas the activity of the STAT5a/cyclin D1 promoter was unaffected under hypoxic conditions. These increases in promoter activity are predominantly mediated by the Jak2/ STAT5b signaling pathway. We have shown by EMSA that hypoxia induces STAT5 to bind to the cyclin D1 promoter (GAS-1) in MCF-7 and HC11 cells. These data suggest that STAT5b may mediate the transcriptional activation of cyclin D1 after hypoxic stimulation.

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Iron deprivation‐induced apoptosis in HL‐60 cells

Cited by 86 publications

References 6 publications

Virus and siderophore-mediated transfer of available Fe between heterotrophic bacteria: characterization using an Fe-specific bioreporter

Virus and siderophore-mediated transfer of available Fe between heterotrophic bacteria: characterization using an Fe-specific bioreporter

Dysregulation of ferroportin 1 interferes with spleen organogenesis in polycythaemia mice

Hypoxia activates the cyclin D1 promoter via the Jak2/STAT5b pathway in breast cancer cells

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