Iron deficiency upregulates Egr1 expression

Lee, Seung Min; Lee, Sun Bok; Prywes, Ron; Vulpe, Chris D.

doi:10.1007/s12263-015-0468-0

Cited by 9 publications

(5 citation statements)

References 38 publications

(33 reference statements)

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“…In contrast, mRNA levels of early growth response 1 (Egr1) were ∼11‐fold upregulated by DFO (Supporting Information Fig. 2), as expected . Egr1 induction is involved in the transactivation of hypoxia‐inducible factor 1α (HIF‐1α) , which is a transcription factor activated by DFO .…”

Section: Resultssupporting

confidence: 60%

Deferoxamine stimulates LDLR expression and LDL uptake in HepG2 cells

Guillemot

Asselin

Susan‐Resiga

et al. 2015

Molecular Nutrition Food Res

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Section: Resultssupporting

confidence: 60%

Deferoxamine stimulates LDLR expression and LDL uptake in HepG2 cells

Guillemot

Asselin

Susan‐Resiga

et al. 2015

Molecular Nutrition Food Res

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“…Interestingly, the iron chelator deferoxamine (DFO) caused a dramatic upregulation of ERK phosphorylation similar to effects previously reported with other iron chelators (Figure 4E,F). 16 …”

Section: Resultsmentioning

confidence: 99%

Identification and initial characterization of a potent inhibitor of ferroptosis

Kuganesan

Dlamini

McDaniel

et al. 2020

J of Cellular Biochemistry

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Ferroptosis is a form of iron‐dependent cell death characterized by elevated lipid peroxides and reactive oxygen species (ROS). Glutathione (GSH) plays an essential role in scavenging ROS to maintain cell viability and acts as a cofactor of GSH peroxidase 4 (GPX4) that protects lipids from oxidation. We have previously described a novel class of small molecules that induce ferroptosis in certain types of cancer cells. These compounds induce ferroptosis by blocking the uptake of cystine required for GSH synthesis. Even though ferroptosis is a well‐established form of cell death, signaling pathways that modulate this process are not known. Therefore, we used a panel of growth factors/kinase inhibitors to test effects on ferroptosis induced by our lead compound. We discovered that BMS536924, a dual inhibitor of insulin‐like growth and insulin receptors, is a potent inhibitor of ferroptosis. Further investigation indicated that the anti‐ferroptotic activity of BMS536924 does not lie in its ability to inhibit insulin signal transduction. Instead, we provide evidence that BMS536924 binds iron, an essential cofactor in ferroptosis. Our results suggest caution in interpreting the effects of BMS536924 in investigations of insulin signaling and uncover a novel ferroptosis inhibitor.

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“…1B ) tissues, as compared to the CON rats. The TfR and ferritin levels are reciprocally regulated in response to iron status [ 19 20 21 ]. Similar to changes in tissue iron concentrations, iron repletion significantly increased the ferritin protein levels in both liver and spleen tissues compared with the ID rats, but did not reach to the levels found in the CON rats ( Fig.…”

Section: Resultsmentioning

confidence: 99%

Effects of developmental iron deficiency and post-weaning iron repletion on the levels of iron transporter proteins in rats

Shin

Chung

2015

Nutr Res Pract

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BACKGROUND/OBJECTIVESIron deficiency in early life is associated with developmental problems, which may persist until later in life. The question of whether iron repletion after developmental iron deficiency could restore iron homeostasis is not well characterized. In the present study, we investigated the changes of iron transporters after iron depletion during the gestational-neonatal period and iron repletion during the post-weaning period.MATERIALS/METHODSPregnant rats were provided iron-deficient (< 6 ppm Fe) or control (36 ppm Fe) diets from gestational day 2. At weaning, pups from iron-deficient dams were fed either iron-deficient (ID group) or control (IDR group) diets for 4 week. Pups from control dams were continued to be fed with the control diet throughout the study period (CON).RESULTSCompared to the CON, ID rats had significantly lower hemoglobin and hematocrits in the blood and significantly lower tissue iron in the liver and spleen. Hepatic hepcidin and BMP6 mRNA levels were also strongly down-regulated in the ID group. Developmental iron deficiency significantly increased iron transporters divalent metal transporter 1 (DMT1) and ferroportin (FPN) in the duodenum, but decreased DMT1 in the liver. Dietary iron repletion restored the levels of hemoglobin and hematocrit to a normal range, but the tissue iron levels and hepatic hepcidin mRNA levels were significantly lower than those in the CON group. Both FPN and DMT1 protein levels in the liver and in the duodenum were not different between the IDR and the CON. By contrast, DMT1 in the spleen was significantly lower in the IDR, compared to the CON. The splenic FPN was also decreased in the IDR more than in the CON, although the difference did not reach statistical significance.CONCLUSIONSOur findings demonstrate that iron transporter proteins in the duodenum, liver and spleen are differentially regulated during developmental iron deficiency. Also, post-weaning iron repletion efficiently restores iron transporters in the duodenum and the liver but not in the spleen, which suggests that early-life iron deficiency may cause long term abnormalities in iron recycling from the spleen.

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Iron deficiency upregulates Egr1 expression

Cited by 9 publications

References 38 publications

Deferoxamine stimulates LDLR expression and LDL uptake in HepG2 cells

Deferoxamine stimulates LDLR expression and LDL uptake in HepG2 cells

Identification and initial characterization of a potent inhibitor of ferroptosis

Effects of developmental iron deficiency and post-weaning iron repletion on the levels of iron transporter proteins in rats

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