Iron-induced Damage in Corpus Striatal Cells of Neonatal Rats: Attenuation by Folic Acid

Saadeldien, Heba M.; Mohamed, Aml; Hussein, Mahmoud R.

doi:10.3109/01913123.2011.630125

Cited by 3 publications

(3 citation statements)

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“…In this regard, it was interesting to observe a relationship between higher transferrin saturation and increased CD8 + T-cell apoptosis. Iron induced apoptosis had been already reported in human hepatocytes and rat neurons but it had never been described in human lymphocytes [ 37 , 38 ]. It could be speculated that in this way iron overload could contribute to the decreased numbers of CD8 + T cells in HH.…”

Section: Discussionmentioning

confidence: 99%

Lymphocyte Gene Expression Signatures from Patients and Mouse Models of Hereditary Hemochromatosis Reveal a Function of HFE as a Negative Regulator of CD8+ T-Lymphocyte Activation and Differentiation In Vivo

et al. 2015

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Abnormally low CD8+ T-lymphocyte numbers is characteristic of some patients with hereditary hemochromatosis (HH), a MHC-linked disorder of iron overload. Both environmental and genetic components are known to influence CD8+ T-lymphocyte homeostasis but the role of the HH associated protein HFE is still insufficiently understood. Genome-wide expression profiling was performed in peripheral blood CD8+ T lymphocytes from HH patients selected according to CD8+ T-lymphocyte numbers and from Hfe -/- mice maintained either under normal or high iron diet conditions. In addition, T-lymphocyte apoptosis and cell cycle progression were analyzed by flow cytometry in HH patients. HH patients with low CD8+ T-lymphocyte numbers show a differential expression of genes related to lymphocyte differentiation and maturation namely CCR7, LEF1, ACTN1, NAA50, P2RY8 and FOSL2, whose expression correlates with the relative proportions of naïve, central and effector memory subsets. In addition, expression levels of LEF1 and P2RY8 in memory cells as well as the proportions of CD8+ T cells in G2/M cell cycle phase are significantly different in HH patients compared to controls. Hfe -/- mice do not show alterations in CD8+ T-lymphocyte numbers but differential gene response patterns. We found an increased expression of S100a8 and S100a9 that is most pronounced in high iron diet conditions. Similarly, CD8+ T lymphocytes from HH patients display higher S100a9 expression both at the mRNA and protein level. Altogether, our results support a role for HFE as a negative regulator of CD8+ T-lymphocyte activation. While the activation markers S100a8 and S100a9 are strongly increased in CD8+ T cells from both, Hfe -/- mice and HH patients, a differential profile of genes related to differentiation/maturation of CD8+ T memory cells is evident in HH patients only. This supports the notion that HFE contributes, at least in part, to the generation of low peripheral blood CD8+ T lymphocytes in HH.

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Section: Discussionmentioning

confidence: 99%

Lymphocyte Gene Expression Signatures from Patients and Mouse Models of Hereditary Hemochromatosis Reveal a Function of HFE as a Negative Regulator of CD8+ T-Lymphocyte Activation and Differentiation In Vivo

et al. 2015

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“…Although the underlying mechanism of this therapy is not completely understood (Copp et al, 2013). We hypothesized a possible connection between folic acid supplementation and HO-1 based on the work of Saadeldien and others, who demonstrated that folic acid reduced oxidative damage from iron supplementation in neonatal rodent neuronal tissues (Saadeldien et al, 2012). Since we did not have data on folic acid supplementation in early pregnancy, the additional hypothesis about a modifying influence between folate and HO-1 variants could not be tested.…”

Section: Discussionmentioning

confidence: 99%

Heme oxygenase‐1 promoter polymorphisms and risk of spina bifida

Fujioka

Yang

Wallenstein

et al. 2015

Birth Defects Research

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“…GFAP staining was also slightly reduced in FA-treated pregnant rats. Saadeldien et al 49 found that maternal FA intake reduced iron-induced oxidative stress damage and GFAP expression levels in striatal tissue. Accordingly, we also observed decreased cortical GFAP expression in seizure-induced prepubertal rats born to FA-treated mothers ( Fig.…”

Section: U N C O R R E C T E D P R O O Fmentioning

confidence: 99%

Gestational treatment of folic acid attenuates blood–brain barrier leakage in pregnant- and prepubertal rats after pentylenetetrazole-induced seizure

Seker¹,

Yorulmaz²,

Kaptan³

et al. 2014

Nutritional Neuroscience

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Iron-induced Damage in Corpus Striatal Cells of Neonatal Rats: Attenuation by Folic Acid

Abstract: Intake of folic acid can protect the neonatal striatal tissue against iron-induced oxidative stress damage.

Cited by 3 publications

References 62 publications

Lymphocyte Gene Expression Signatures from Patients and Mouse Models of Hereditary Hemochromatosis Reveal a Function of HFE as a Negative Regulator of CD8+ T-Lymphocyte Activation and Differentiation In Vivo

Lymphocyte Gene Expression Signatures from Patients and Mouse Models of Hereditary Hemochromatosis Reveal a Function of HFE as a Negative Regulator of CD8+ T-Lymphocyte Activation and Differentiation In Vivo

Heme oxygenase‐1 promoter polymorphisms and risk of spina bifida

Gestational treatment of folic acid attenuates blood–brain barrier leakage in pregnant- and prepubertal rats after pentylenetetrazole-induced seizure

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