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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk

ABSTRACT: To determine the physiological roles of ZIP10 and zinc in erythroid progenitor cells, Zip10 was depleted via nucleofector-mediated siRNA delivery into cells and cellular zinc was restricted by DTPA treatment. The transcriptome profiles acquired from RNA-seq were compared with those of control cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE310594 | GEO | 2025/11/19

REPOSITORIES: GEO

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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk II

Project description:To determine the physiological roles of zinc in erythroid progenitor cells, cellular zinc was restricted by 50 µM DTPA treatment (a zinc chelator) for 24 hours in differentiating G1E-ER4 cells. G1E-ER4 cells induced for differentiation by beta-estradiol were divided into two groups: control and 50 µM DTPA treatment. A sample from cells untreated with beta-estradiol was also included as an undifferentiated group.

2025-11-19 | GSE310207 | GEO

Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk I

Project description:To determine the effects of heme synthesis inhibition via different pathways in erythroid progenitor cells, heme synthesis was inhibited by 50 µM DTPA treatment (a zinc chelator), 50 µM DFO treatment (a iron chelator), or 0.2 mM succinylacetone (SA, a ALAD inhibitor) for 24 hours in differentiating G1E-ER4 cells. G1E-ER4 Cells were divided into four groups: untreated control, 50 µM DTPA treatment, 50 µM DFO treatment, and 0.2 mM SA. The transcriptome profiles acquired from RNA-seq were compared with those of control cells.

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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk

Project description:Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk

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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk II

Project description:Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk II

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Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk I

Project description:Nutrigenomic profiling identifies ZIP10 (SLC39A10) as a regulator of erythroid zinc homeostasis with genetic associations to anemia risk I

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Endometrial zinc transporter Slc39a10/Zip10 is indispensable for progesterone responsiveness and successful pregnancy in mice

Project description:To investigate the molecular mechanism underlying zinc transporter in the endometrium during embryo implantation, we generated mice with uterine-specific deletion of one of zinc transporter, Zip10. We report the sequencing of the uterine transcriptome of control and uterine-specific Zip10-deficient mice at day 4 (1600h) of pregnancy.

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Zinc transporters ZnT1 (Slc30a1), Zip8 (Slc39a8), and Zip10 (Slc39a10) in mouse red blood cells are differentially regulated during erythroid development and by dietary zinc deficiency.

Project description:Zinc is essential for normal erythroid cell functions and therefore intracellular zinc homeostasis during erythroid differentiation is tightly regulated. However, a characterization of zinc transporters in erythrocytes has not been conducted. The membrane fraction of mature mouse RBC was screened for zinc transporter expression using western analysis as a first step in the characterization process. ZnT1, Zip8, and Zip10 were detected among the 12 transporter proteins tested. We examined expression of these zinc transporters during erythropoietin (EPO)-induced differentiation of splenic erythroid progenitor cells into reticulocytes. Both Zip8 and Zip10 mRNA increased by 2-6 h after addition of EPO to the cells. In contrast, maximal RNA levels for the zinc transporter ZnT1 and erythroid delta-aminolevulinic acid synthase were only produced by 24 h after EPO. We confirmed these changes in transcript abundance by western analysis. Dietary zinc status influences zinc-dependent functions of RBC. To determine whether the identified zinc transporters respond to dietary zinc status, mice were fed a zinc-deficient or control diet. Incorporation of (65)Zn into erythrocytes in vitro was significantly increased in cells from the zinc-deficient mice. Western analysis and densitometry revealed that erythrocyte Zip10 was upregulated and ZnT1 was downregulated in the zinc-depleted mice. Zip8 was not affected by restricted zinc intake. Collectively, these data suggest that the zinc transporters ZnT1, Zip8, and Zip10 are important for zinc homeostasis in erythrocytes and that ZnT1 and Zip10 respond to the dietary zinc supply.

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Project description:The Affymetrix Human Gene 2.0 ST array was used to measure differential expression of RNA isolated from normal and Diamond Blackfan anemia (DBA) erythroid progenitors after ex vivo expansion of circulating, peripheral blood derived hematopoietic stem cells under erythroid growth conditions. The gene-level probe summaries reported in this series were computed using RMA as implemented in the Bioconductor package Oligo v1.36.1. Diamond Blackfan anemia (DBA) is a congenital bone marrow failure syndrome characterized by erythroid aplasia, usually without perturbation of other hematopoietic lineages. Approximately 65% of DBA patients with autosomal dominant inheritance have heterozygous mutations or deletions in ribosomal protein (RP) genes while <1% of patients with X-linked inheritance have been identified with mutations in the transcription factor, GATA1. Erythroid cells from patients with DBA have not been well characterized and the mechanisms underlying the erythroid specific effects of either RP or GATA1 associated DBA remain unclear. We have developed an in vitro culture system to expand peripheral blood CD34+ progenitor cells from patients with DBA and differentiate them into erythroid cells. Cells from patients with RP or GATA1 mutations showed decreased proliferation and delayed erythroid differentiation compared to controls. RNA transcript analyses of erythroid cells from controls and patients with RP or GATA1 mutations showed distinctive differences, with upregulation of heme biosynthesis genes prominently in RP-mediated DBA and failure to upregulate components of the translational apparatus in GATA1-mediated DBA. Our data show that dysregulation of translational function is a common feature of DBA caused by both RP and GATA1 mutations.

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Requirement of zinc transporter ZIP10 for epidermal development: Implication of the ZIP10-p63 axis in epithelial homeostasis.

Project description:Skin tissues, in particular the epidermis, are severely affected by zinc deficiency. However, the zinc-mediated mechanisms that maintain the cells that form the epidermis have not been established. Here, we report that the zinc transporter ZIP10 is highly expressed in the outer root sheath of hair follicles and plays critical roles in epidermal development. We found that ZIP10 marked epidermal progenitor cell subsets and that ablating Zip10 caused significant epidermal hypoplasia accompanied by down-regulation of the transactivation of p63, a master regulator of epidermal progenitor cell proliferation and differentiation. Both ZIP10 and p63 are significantly increased during epidermal development, in which ZIP10-mediated zinc influx promotes p63 transactivation. Collectively, these results indicate that ZIP10 plays important roles in epidermal development via, at least in part, the ZIP10-zinc-p63 signaling axis, thereby highlighting the physiological significance of zinc regulation in the maintenance of skin epidermis.

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