Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA407205 | ENA |
REPOSITORIES: ENA
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Project description:<p>The effects of iron deficiency (ID) during infancy extend beyond the hematologic compartment and include short- and long-term adverse effects on many tissues including the brain. However, sensitive biomarkers of iron-dependent brain health are lacking in humans. To determine whether serum and cerebrospinal fluid (CSF) biomarkers of ID-induced metabolic dysfunction are concordant in the pre/early anemic stage of ID before anemia in a nonhuman primate model of infantile iron deficiency anemia (IDA). ID (n = 7), rhesus infants at 4 mo (pre-anemic period) and 6 mo of age (anemic) were examined. Hematological, metabolomic and proteomic profiles were generated via HPLC/MS at both time points to discriminate serum biomarkers of ID-induced brain metabolic dysfunction. We identified 227 metabolites and 205 proteins in serum. Abnormalities indicating altered liver function, lipid dysregulation and increased acute phase reactants were present in ID. In CSF, we measured 210 metabolites and 1560 proteins with changes in ID infants indicative of metabolomic and proteomic differences indexing disrupted synaptogenesis. Systemic and CSF proteomic and metabolomic changes were present and concurrent in the pre-anemic and anemic periods. Multiomic serum and CSF profiling uncovered pathways disrupted by ID in both the pre-anemic and anemic stages of infantile IDA, including evidence for hepatic dysfunction and activation of acute phase response. Parallel changes observed in serum and CSF potentially provide measurable serum biomarkers of ID that reflect at-risk brain processes prior to progression to clinical anemia.</p><p><br></p><p><strong>Data availability:</strong></p><p>The proteomics data have been deposited into the ProteomeXchange Consortium via the PRIDE partner repository with the data set identifier <a href='https://www.ebi.ac.uk/pride/archive/projects/PXD028275' rel='noopener noreferrer' target='_blank'>PXD028275</a>.</p>
2022-07-12 | MTBLS3388 | MetaboLights
Project description:Compromised renal function after renal allograft transplantation often results in anemia in the recipient. Molecular mechanisms leading to anemia during acute rejection are not fully understood; inadequate erythropoietin production and iron deficiency have been reported to be the main contributors. To increase our understanding of the molecular events underlying anemia in acute rejection, we analyzed the gene expression profiles of peripheral blood lymphocytes (PBL) from four pediatric renal allograft recipients with acute rejection and concurrent anemia, using DNA microarrays containing 9000 human cDNA clones (representing 7469 unique genes). In these anemic rejecting patients, an 'erythropoiesis cluster' of 11 down-regulated genes was identified, involved in hemoglobin transcription and synthesis, iron and folate binding and transport. Additionally, some alloimmune response genes were simultaneously down-regulated. An independent data set of 36 PBL samples, some with acute rejection and some with concurrence of acute rejection and anemia, were analyzed to support a possible association between acute rejection and anemia. In conclusion, analysis using DNA microarrays has identified a cluster of genes related to hemoglobin synthesis and/or erythropoeisis that was altered in kidneys with renal allograft rejection compared with normal kidneys. The possible relationship between alterations in the expression of this cluster, reduced renal function, the alloimmune process itself, and other influences on the renal transplant awaits further analysis.
2005-11-01 | E-SMDB-2730 | biostudies-arrayexpress
Project description:Tmprss6 is the master inhibitor of hepcidin and its inactivation causes iron refractory iron deficiency anemia both in human and in mice. Mice with iron deficiency anemia (IDA)-low hepcidin show a pro-inflammatory response that is blunted in iron deficienct-high hepcidin Tmprss6 null mice. We investigated the transcriptional response associated with chronic hepcidin overexpression by comparing whole genome transcription profiling of the liver of Tmprss6 KO mice and IDA animals, irrespective of iron deficiency. Total liver RNA obtained from Tmprss6 KO mice were compared to wild type (iron deficient) animals, under basal conditions and after LPS challenge
2013-10-09 | E-GEOD-46287 | biostudies-arrayexpress
Project description:Tmprss6 is the master inhibitor of hepcidin and its inactivation causes iron refractory iron deficiency anemia both in human and in mice. Mice with iron deficiency anemia (IDA)-low hepcidin show a pro-inflammatory response that is blunted in iron deficienct-high hepcidin Tmprss6 null mice. We investigated the transcriptional response associated with chronic hepcidin overexpression by comparing whole genome transcription profiling of the liver of Tmprss6 KO mice and IDA animals, irrespective of iron deficiency.
2013-10-09 | GSE46287 | GEO
Project description:The microarray gene expression pattern was studied using 798 different cancer cell lines. The cancer cell lines are obtained from different centers. Annotation information were provided in the supplementary file. golub-00327 Assay Type: Gene Expression Provider: Affymetrix Array Designs: HT_HG-U133A Organism: Homo sapiens (ncbitax) Tissue Sites: leukemia, Urinary tract, Lung, BiliaryTract, Autonomic Ganglion, Thyroid gland, Stomach, Breast, Pancreas, Head and Neck, Lymphoma, Colorectal, Placenta, Liver, Brain, Bone, pleura, Skin, endometrium, Ovary, cervix, Oesophagus, Connective and Soft Tissue, Muscle, Kidney, Prostate, Adrenal Gland, Eye, Testis, Smooth Muscle Tissue, Vulva, Unknow Material Types: cell, synthetic_RNA, whole_organism, total_RNA, BVG Disease States: M3 acute myeloid leukemia, hairy cell leukemia, transitional cell carcinoma, Adenocarcinoma, B cell lymphoma unspecified, Acute Lymphoblastic Leukemia, blast phase chronic myeloid leukemia, Carcinoma, M6 acute myeloid leukemia, Neuroblastoma, follicular carcinoma, ductal carcinoma, Burkitt Lymphoma, Squamous Cell Carcinoma, M5 acute myeloid leukemia, Mycosis Fungoides and Sezary Syndrome, Acute T-Cell Lymphoblastic Leukemia, Adult T-Cell Leukemia/Lymphoma, M2 Therapy-Related Myeloid Neoplasm, Choriocarcinoma, Plasma Cell Myeloma, Hepatocellular Carcinoma, anaplastic large cell lymphoma, primitive neuroectodermal tumor-medulloblastoma, M4 acute myeloid leukemia, B Acute Lymphoblastic Leukemia, Acute Leukemia of Ambiguous Lineage, Osteosarcoma, Hodgkin Lymphoma, Mesothelioma, chondrosarcoma, Glioblastoma Multiforme, Malignant Melanoma, carcinosarcoma-malignant mesodermal mixed tumor, bronchioloalveolar adenocarcinoma, chronic lymphocytic leukemia-small lymphocytic lymphoma, micropapillary carcinoma, diffuse large B cell lymphoma, myelodysplastic syndrome, giant cell carcinoma, teratoma, multipotential sarcoma, Small Cell Carcinoma, ASTROCYTOMA, Fibrosarcoma, mucoepidermoid carcinoma, Rhabdomyosarcoma, L1 Acute T-Cell Lymphoblastic Leukemia, Glioma, Anaplastic Astrocytoma, Non-small cell carcinoma, Large Cell Carcinoma, mucinous carcinoma, Acute Myeloid Leukemia, malignant fibrous histiocytoma-pleomorphic sarcoma, clear cell carcinoma, B cell lymphoma unspecified, Anaplastic Carcinoma, Ewings sarcoma-peripheral primitive neuroectodermal tumor, undifferentiated carcinoma, Sarcoma, Embryonal Rhabdomyosarcoma, epithelioid sarcoma, renal cell carcinoma, carcinoid-endocrine tumor, Synovial Sarcoma, lymphoid neoplasm, rhabdoid tumor, Refractory Anemia with Excess Blasts, Liposarcoma, biphasic mesothelioma, adrenal cortical carcinoma, adenosquamous carcinoma, L2 Acute T-Cell Lymphoblastic Leukemia, chronic myeloid leukemia, Micropapillary Serous Carcinoma, desmoplastic, acute leukemia, Retinoblastoma, teratocarcinoma, clear cell renal cell carcinoma, Follicular Lymphoma, Wilms Tumor, M7 acute myeloid leukemia, gliosarcoma, embryonal carcinoma, Leiomyosarcoma, medullary carcinoma, granulosa cell tumor, papillary carcinoma, NS Acute Lymphoblastic Leukemia, papillary transitional cell carcinoma, small cell adenocarcinoma, epithelial dysplasia, hyperplasia, tubular adenocarcinoma, metaplasia, papillary ductal carcinoma, chronic eosinophilic leukemia-hypereosinophilic syndrome, #N/A, malignant trichilemmal cyst, Medullary Breast Carcinoma, L2 Acute Lymphoblastic Leukemia, Osteoblastic Osteosarcoma
2015-05-16 | E-GEOD-68950 | biostudies-arrayexpress
Project description:The mechanism underlying thrombocytosis in patients with iron deficiency anemia remains unknown. We present findings that support the hypothesis that low iron biases the commitment of Megakaryocytic-Erythroid Progenitors (MEP) toward the megakaryocytic (Mk) lineage in mice. In MEP of Transmembrane serine protease 6 knockout (Tmprss6-/-) mice, which exhibit iron deficiency microcytic anemia concomitant with thrombocytosis, we observed a megakaryocytic (Mk) bias, decreased labile iron, and decreased proliferation relative to wild-type (WT) MEP. Bone marrow transplantation assays suggest that the systemic iron deficiency of the Tmprss6-/- recipients contributes to the MEP lineage commitment bias. Genes involved in metabolic, VEGF, and ERK pathways were enriched among those differentially expressed between WT and Tmprss6-/- MEP. Corroborating our findings from the murine model of chronic iron deficiency anemia, primary human MEP also exhibited decreased proliferation and Mk-biased commitment when their iron sensing pathways were disrupted by knockdown of Transferrin Receptor 2. These data are consistent with a model in which low iron in the marrow environment affects MEP metabolism, attenuates ERK signaling, slows proliferation, and biases MEP toward Mk lineage commitment. Keywords: megakaryocytic-erythroid progenitor (MEP), iron deficiency, Tmprss6
2023-03-17 | GSE227563 | GEO
Project description:Cardiac transcriptome in iron-deficiency anemia
| PRJNA682047 | ENA
Project description:Prospective study to test whether the immunochemical fecal occult blood test (FIT) for colorectal cancer (CRC) helps to prioritize patients with iron deficiency anemia for colonoscopy.
| 2216665 | ecrin-mdr-crc
Project description:Epigenetic dysregulation is a common feature of acute myeloid leukemia (AML). Recently it has become clear that long noncoding RNAs (lncRNAs) can play a key role in epigenetic regulation, and consequently also dysregulation. Currently, our understanding of the requirements and roles of lncRNAs in AML is still limited. Using CRISPRi screening, we identified the lncRNA SGOL1-AS1 as an essential regulator of survival in THP-1 AML cells. We use RNA affinity purification using a biotinylated bait to pull down binding partners of the lncRNA, SGOL1-AS1. The identified proteins show a signficant enrichment for chromatin-modifying proteins involved in gene repression and chromosome organization.
2023-06-12 | PXD034329 | Pride
Project description:Differentiating agents have been proposed to overcome the impaired cellular differentiation in acute myeloid leukemia (AML). However, only the combinations of all-trans retinoic acid or arsenic trioxide with chemotherapy have been successful, and only in treating acute promyelocytic leukemia (also called AML3). Here we showed that iron homeostasis is an effective target in the treatment of AML. Iron chelating therapy induces the differentiation of leukemia blasts and normal bone marrow precursors into monocytes/macrophages in a manner involving modulation of reactive oxygen species expression and the activation of mitogen-activated protein kinases (MAPK). Thirty percent of the genes most strongly induced by iron deprivation are also targeted by vitamin D3 (VD), a well-known differentiating agent. Iron chelating agents induce expression and phosphorylation of the VD receptor, and iron deprivation and VD act synergistically. VD magnifies activation of MAPK JNK and the induction of VD receptor target genes. When used to treat one AML patient refractory to chemotherapy, the combination of iron chelating agents and VD resulted in reversal of pancytopenia and blast differentiation. We propose that iron availability modulates myeloid cell commitment, and that targeting this cellular differentiation pathway together with conventional differentiating agents provides new therapeutic modalities for AML. This study presents 8 arrays 4x44K Agilent.
2010-03-23 | E-TABM-925 | biostudies-arrayexpress