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Mesendoderm differentiation with Hif-1a overexpression and knockdown under normoxia or hypoxia

ABSTRACT: mesendoderm differentiation with Hif-1a overexpression and knockdown under normoxia or hypoxia

PROVIDER: PRJNA858086 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20111500_1.fastq.gz	Fastqsanger.gz
	SRR20111500_2.fastq.gz	Fastqsanger.gz
	SRR20111501_1.fastq.gz	Fastqsanger.gz
	SRR20111501_2.fastq.gz	Fastqsanger.gz
	SRR20111502_1.fastq.gz	Fastqsanger.gz

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mesendoderm differentiation with Hif-1a overexpression and knockdown under normoxia or hypoxia

Project description:To study the gene expression profile in the mesendoderm differerntiation of control and Hif-1a overexpression, we performed RNA-seq on the total RNA samples collected from the differentiation of control and Hif-1a overexpression AB2.2 mESCs at differentiation day 4.In addition, to study the gene expression profile in the mesendoderm differerntiation of Hif-1a knockdown under normoxia and hypoxia, we performed RNA-seq on the total RNA samples collected from the differentiation of Hif-1a knockdown AB2.2 mESCs under normoxia or hypoxia at differentiation day 4. Cell lines were built by infecting AB2.2 cells with lentiviruses. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.

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Global genomic profiling of HIF-1a-regulated genes in bone marrow B cells under hypoxia or normoxia

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Identification of hypoxia regulated HIF-1A and HIF-2A specific target genes in Glioblastoma

Project description:HIF-1A and HIF-2A regulate both overlapping and unique target genes in response to hypoxia. In this dataset, we identify specific HIF-1A and HIF-2A target genes in glioblastoma cells. 12 samples were analysed comprising 4 experimental conditions (normoxia scr, hypoxia scr, hypoxia siHIF1, hypoxia siHIF2) in triplicate. We made pairwise comparisons between the averages of each triplicate set to normoxia scr using the Partek suite.

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mesendoderm differentiation with Hif-1a knockdown

Project description:To study the gene expression profile in the mesendoderm differerntiation of scramble control and Hif-1a knockdown, we performed RNA-seq on the total RNA samples collected from the differentiation of scramble and Hif-1a knockdown AB2.2 mESCs at differentiation day 4. Sramble and Hif-1a knockdown AB2.2 mESCs were built by infecting AB2.2 cells with lentiviruses. Each group contained three biological replicates. The expression matrix was obtained by Hisat2 followed by Stringtie.

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mesendoderm differentiation with Hif-1a knockdown

Project description:mesendoderm differentiation with Hif-1a knockdown

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Identification of hypoxia regulated HIF-1A and HIF-2A specific target genes in Glioblastoma

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Defective mitochondrial cardiolipin remodeling dampens HIF-1a expression in hypoxia

Project description:Mitochondria fulfill vital metabolic functions and act as crucial cellular signaling hubs integrating their metabolic status into the cellular context. Here, we show that defective cardiolipin-remodeling, upon loss of the cardiolipin acyl transferase Tafazzin, mutes HIF-1a signaling in hypoxia. Tafazzin-deficiency does not affect posttranslational HIF-1a regulation but rather HIF-1a gene-expression, a dysfunction recapitulated in iPSCs-derived cardiomyocytes from Barth Syndrome patients with Tafazzin-deficiency. RNAseq analyses confirmed drastically altered signaling in Tafazzin mutant cells. In hypoxia, Tafazzin-deficient cells display reduced production of reactive oxygen species (ROS) perturbing NF-kB activation and concomitantly HIF-1a gene-expression. In agreement, Tafazzin-deficient mice hearts display reduced HIF-1a levels and undergo maladaptive hypertrophy with heart failure in response to pressure overload challenge. We conclude that defective mitochondrial cardiolipin-remodeling dampens HIF-1a signaling through inactivation of a non-canonical signaling pathway: Lack of NF-kB activation through reduced mitochondrial ROS production diminishes HIF-1a transcription.

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Project description:Recently, hypoxia via the transcription factor HIF-1a has been implicated to play an important role for the fate of the adaptive immune response by regulatory T cells (Treg) and T helper 17 cells (TH17) in the mouse model. However, the reports on the effect of HIF-1a are conflicting and so far no functional data in the human system are available. Therefore, we analyzed the effect of hypoxia and HIF-1a on Treg and TH17 in the human system. FACS, western blot and reporter assays clearly demonstrated that hypoxia does not up-regulate the level of HIF-1a in CD4+ T cells (THC) and microarray analysis revealed no change of the transcriptome comparing normoxia vs. hypoxia. Furthermore, we could show that HIF-1a is almost exclusively regulated via NF-kB and NFAT, whereas hydroxylation and subsequent degradation of HIF-1a had little to no effect. In addition, we showed that HIF-1a is essential for nTreg mediated suppression and for IL-17A secretion of TH17, but not for TH17 lineage commitment measured by RORÎ³t expression. In conclusion, our results demonstrated that THC have a distinct regulation of HIF-1a protein levels, which was absolutely essential for Treg and TH17 function. 3 patients, 2 cell type, 2 treatments = 12 arrays

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Project description:Recently, hypoxia via the transcription factor HIF-1a has been implicated to play an important role for the fate of the adaptive immune response by regulatory T cells (Treg) and T helper 17 cells (TH17) in the mouse model. However, the reports on the effect of HIF-1a are conflicting and so far no functional data in the human system are available. Therefore, we analyzed the effect of hypoxia and HIF-1a on Treg and TH17 in the human system. FACS, western blot and reporter assays clearly demonstrated that hypoxia does not up-regulate the level of HIF-1a in CD4+ T cells (THC) and microarray analysis revealed no change of the transcriptome comparing normoxia vs. hypoxia. Furthermore, we could show that HIF-1a is almost exclusively regulated via NF-kB and NFAT, whereas hydroxylation and subsequent degradation of HIF-1a had little to no effect. In addition, we showed that HIF-1a is essential for nTreg mediated suppression and for IL-17A secretion of TH17, but not for TH17 lineage commitment measured by RORγt expression. In conclusion, our results demonstrated that THC have a distinct regulation of HIF-1a protein levels, which was absolutely essential for Treg and TH17 function.

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Project description:Based on the results of numerous clinical and preclinical analyses, the transcription factor HIF-1a has been identified as an important tumor-promoting factor and is considered to be an attractive target for cancer therapy. To further deconstruct the molecular nature of HIF-1a’s role in tumorigenesis, we have applied lentiviral shRNA transduction to establish HIF-1a-deficient gastric cancer cells. Interestingly, functional analyses failed to show a significant growth defect of HIF-1a-deficient gastric cancer cells in vitro and in vivo. These observations led us to propose that stable inactivation of HIF-1a resulted in efficient compensation enabling cell growth and, ultimately, tumor progression in a HIF-1a-independent manner. To better understand the mechanisms that control this compensation, we performed transcriptomics of control (“scrambled” (SCR)) and HIF-1a-deficient (HIF) gastric cancer cells. Analysis of hypoxia-inducible factor-1alpha (HIF-1a)-deficient gastric cancer cells under normoxia. The transcription factor HIF-1a is a key regulator of oxygen homeostasis and has been identified as an important tumor-promoting factor. Results provide insight into the role of HIF-1a in gastric carcinogenesis.

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