Dichelostemma ida-maia
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ABSTRACT:
PROVIDER: PRJNA197399 | ENA |
REPOSITORIES: ENA
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Project description:Background Gastric Helicobacter pylori colonization leads to iron deficiency anemia (IDA), especially in children and adolescents. However the pathogenesis is poorly understood. Objective We sought to identify specific H. pylori genes involved in IDA development, by comparing bacterial genome-wide expression profiling in patients affected or not. Methods H. pylori were isolated from four children with IDA and four from matched controls without IDA. Based on these isolates, cDNA microarrays under iron-replete or depleted conditions were systematically performed to compare gene expression profiles at the whole genome level. Real-time reverse-transcription (RT-) PCR and protein assays were performed for further assessing the profile differentiation of the identified H. pylori IDA-associated genes. Results We identified 29 and 11 genes with significantly higher or lower expression in the IDA isolates compared to non-IDA isolates, respectively. Especially notable were higher expression of sabA gene encoding sialic acid-binding adhesin in the IDA isolates, which was confirmed by real-time RT-PCR study. Moreover, iron-depletion in vitro led to up-regulation of fecA1 and frpB1 genes and down-regulation of pfr, as predicted. Known iron-regulated genes such as fur, pfr, fecA, and feoB did not significantly differ between both groups. The IDA isolates had significantly higher expression of vacuolating cytotoxin gene vacA than non-IDA isolates, consistent with the results of VacA protein assays. There were no significant differences in bacterial growth value between IDA and non-IDA isolates. Conclusions It is likely that H. pylori carrying high expression of sabA causes IDA, especially in children and adolescents who have increased daily iron demand. In addition, it is possible that several host-interactive genes, including vacA, may play a synergistic role for sabA in IDA development.
2017-07-25 | GSE101807 | GEO
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:Primary objectives: The primary objective is to investigate circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
Primary endpoints: circulating tumor DNA (ctDNA) via deep sequencing for mutation detection and by whole genome sequencing for copy number analyses before start (baseline) with regorafenib and at defined time points during administration of regorafenib for treatment efficacy in colorectal cancer patients in terms of overall survival (OS).
| 2533916 | ecrin-mdr-crc
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:Forced expression of ASCL1, Nurr1, Lmx1a, miRNA-124 and p53shRNA (ANLmp) in fibroblasts reprograms fibroblasts to induced dopaminergic neurons (iDA). While human lung fibroblasts can be converted rapidly and efficiently, iDA of dermal fibroblast is very unefficient and incompleted. To address this issue, we performed time series RNAseq on both lung and dermal fibroblasts during the first several days of ANLmp induced neuron convertion. Bioinformatics analysis revealed the stable fibroblast gene regulatory network (GRN) was a potential repressive factor for iDA in human dermal fibroblasts.
2019-06-17 | GSE129358 | GEO
Project description:Forced expression of ASCL1, Nurr1, Lmx1a, miRNA-124 and p53shRNA (ANLmp) in fibroblasts reprograms fibroblasts to induced dopaminergic neurons (iDA). While human lung fibroblasts can be converted rapidly and efficiently, iDA of dermal fibroblast is very unefficient and incompleted. To address this issue, we performed time series RNAseq on both lung and dermal fibroblasts during the first four days of ANLmp induced neuron convertion. Bioinformatics analysis revealed the stable fibroblast gene regulatory network (GRN) was a potential repressive factor for iDA in human dermal fibroblasts.
2019-06-17 | GSE125692 | GEO
Project description:Since iron deficiency anemia (IDA) is one of the most common diseases in worldwide, it is an essential issue to prevent and to treat the IDA in public healthcare system. However, the precise adaptive responses and their mechanisms of the hematopoietic system induced by iron deficient state are not fully understood. In this study, low iron diet conditions which induce sever iron deficiency anemia in mice were established. Transcriptome analyses in erythroblasts under normal or iron deficient states were performed to describe the pathological details of IDA. Under iron deficient state, extensive gene expression changes and mitophagy disorder were induced during the terminal maturation of erythroblasts. These findings provide a new insight into pathophysiology and molecular biology of IDA and the function of iron as a coordinator of gene expression networks in erythrocyte maturation.
2016-12-14 | GSE77694 | GEO
Project description:This study identified differentially expressed miRNAs exclusively in invasive ductal adenocarcinoma. The epithelial-mesenchymal transition (EMT) is a critical step for pancreatic cancer cells as an entry of metastatic disease. Wide variety of cytokines and signaling pathways are involved in this complex process while the entire picture is still cryptic. Recently, miRNA was found to regulate cellular function including EMT by targeting multiple mRNAs. We performed comprehensive analysis of miRNA expression profiles in invasive ductal adenocarcinoma (IDA), intraductal papillary mucinous adenoma (IPMA), intraductal papillary mucinous carcinoma (IPMC) and human pancreatic cancer cell line to elucidate essential miRNAs which regulate invasive growth of pancreatic cancer cells. Along with higher expression of miR-21 which has been shown to be highly expressed in IDA, reduced expression of miR-126 in IDA and pancreatic cancer cell line was detected. Re-expression of miR-126 in pancreatic cancer cells resulted in reduced cellular migration, invasion and induction of epithelial marker E-cadherin. We demonstrated for the first time that the miR-126 plays essential role in the inhibition of invasive growth of pancreatic cancer cells.
2011-05-30 | GSE29542 | GEO
Project description:Purpose: We aimed to investigate the effect of several anti-leukemia drugs in combination with decitabine (DAC) on the proliferation of myeloid leukemia cells in vitro and in vivo, to select the most efficient combination group and explore associated mechanisms of these combination therapies. Experimental Design: After comparing with five anti-leukemia drugs in several different kinds of cell lines, the combination effect of idarubicin (IDA) with DAC was best. In vivo, by using microPET, TUNEL, and transmission electron microscopy, the inhibitory effects obtained by sequentially combining DAC with IDA, evidenced by evaluating tumor cell proliferation and cell apoptosis. Molecular studies were conducted using gene chip, which was used to explore associated pathways, and real-time quantitative reverse transcription-PCR, western blot and immunohistochemistry (IHC), used to assess regulation of Wnt/β-catenin pathway. Results: The sequential combination of DAC and IDA showed synergistic induction of cell death in U937, HEL, SKM-1 and cells isolated from AML patients. Importantly, the inhibition of tumor growth in the sequential combination group was found to be significantly higher than that of single drug group or control group in vivo. Moreover, sequential treatment with DAC and IDA induced apoptosis and depression of the Wnt/β-catenin pathway in both culture and animal studies. Conclusions: Our findings showed that sequentially combining decitabine with idarubicin had a synergistic anti-leukemia effect. These findings were attributed to demethylation of Wnt pathway inhibitors and downregulation of Wnt pathway nuclear targets observed in vitro and in vivo. After comparing with five anti-leukemia drugs in several different kinds of cell lines, the combination effect of idarubicin (IDA) with DAC was best. In vivo, by using microPET, TUNEL, and transmission electron microscopy, the inhibitory effects obtained by sequentially combining DAC with IDA, evidenced by evaluating tumor cell proliferation and cell apoptosis. Molecular studies were conducted using gene chip, which was used to explore associated pathways, and real-time quantitative reverse transcription-PCR, western blot and immunohistochemistry (IHC), used to assess regulation of Wnt/β-catenin pathway.
2014-02-13 | E-GEOD-54918 | biostudies-arrayexpress
Project description:Suppression of P53 in conjunction with cell cycle arrest at G1 and appropriate extracellular environment markedly increases the efficiency in the transdifferentiation of human fibroblasts to iDA neurons bt Ascl1, Nurr1, Lmx1a and miR-124.
2015-12-02 | GSE52352 | GEO