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Nguyen2013 - Dynamic model of HIF regulation in hypoxia

ABSTRACT: Its a mathematcial model explaining regulation of HIF via FIH and oxygen. Model is further validated by Experimental data and various hypothesis has been tested on the same.

SUBMITTER: Krishna Kumar Tiwari

PROVIDER: MODEL1912100004 | BioModels | 2019-12-10

REPOSITORIES: BioModels

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			Action	DRS
	MODEL1912100004?filename=Nguyen2013_HIF.cps	Other
	MODEL1912100004?filename=Nguyen2013_HIF.sedml	Other
	MODEL1912100004?filename=Nguyen2013_HIF.xml	Xml

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Publications

A dynamic model of the hypoxia-inducible factor 1α (HIF-1α) network.

Nguyen Lan K LK Cavadas Miguel A S MA Scholz Carsten C CC Fitzpatrick Susan F SF Bruning Ulrike U Cummins Eoin P EP Tambuwala Murtaza M MM Manresa Mario C MC Kholodenko Boris N BN Taylor Cormac T CT Cheong Alex A

Journal of cell science 20130206 Pt 6

Activation of the hypoxia-inducible factor (HIF) pathway is a critical step in the transcriptional response to hypoxia. Although many of the key proteins involved have been characterised, the dynamics of their interactions in generating this response remain unclear. In the present study, we have generated a comprehensive mathematical model of the HIF-1α pathway based on core validated components and dynamic experimental data, and confirm the previously described connections within the predicted ...[more]

PMID: 23390316

Similar Datasets

Nguyen2013 - Dynamic model of HIF regulation in hypoxia (reduced model)

Project description:Its a mathematcial model explaining regulation of HIF via FIH and oxygen. Model is further validated by Experimental data and various hypothesis has been tested on the same.

2019-12-10 | MODEL1912100005 | BioModels

Hypoxia promotes osteonesis via regulation of the mito-nuclear communication [RNA-seq]

Project description:Bone marrow mesenchymal stem cells (MSCs) reside in a hypoxic niche that maintains their differentiation potential. Several studies have highlighted the critical role of hypoxia (low oxygen concentration) in the regulation of stem cell function, reporting differentiation defects following a switch to normoxia (high oxygen concentration). However, the molecular events triggering changes in stem cell fate decisions in response to high oxygen remain elusive. Here, we study the impact of normoxia in the mito-nuclear communication, with regards to stem cell differentiation. We show that normoxia-cultured MSCs undergo profound transcriptional alterations which cause irreversible osteogenesis defects. Mechanistically, high oxygen promotes chromatin compaction and histone hypo-acetylation, particularly on promoters and enhancers of osteogenic genes. Although normoxia induces rewiring of metabolism, resulting in high acetyl-CoA levels, histone hypo-acetylation occurs due to trapping of acetyl-CoA inside mitochondria, likely due to lower CiC activity. Strikingly, restoring the cytosolic acetyl-CoA pool via acetate supplementation remodels the chromatin landscape and rescues the osteogenic defects. Collectively, our results demonstrate that the metabolism-chromatin-osteogenesis axis is heavily perturbed in response to high oxygen and identify CiC as a novel, oxygen-sensitive regulator of MSC function.

2022-10-18 | GSE200070 | GEO

Hypoxia promotes osteonesis via regulation of the mito-nuclear communication [ChIP-seq]

2022-10-18 | GSE200071 | GEO

Hypoxia promotes osteonesis via regulation of the mito-nuclear communication [ATAC-seq]

2022-10-18 | GSE200072 | GEO

Hypoxia-driven histone modifications govern gene regulation for mature eye lens formation

Project description:Evidence suggests that the hypoxic environment of the lens regulates the expression of genes required for lens formation and function. Here, we tested the hypothesis that hypoxia regulates these genes through induction of specific histone modifications. Global levels of hypoxia induced histone modifications were determined in cultured day 13 chick lenses exposed to 1% oxygen. The genome-wide localizations of H3K27ac and H3K4me3 were identified by CUT&RUN analysis and mapped to within 5kb of the transcriptional start sites of genes activated or repressed by hypoxia identified by RNA Seq. The requirement for these histone modifications for hypoxia induced gene expression was determined using inhibitors of histone writers and erasers. The levels of activating modifications H3K4me3, H3K9ac, H3K14ac and H3K27ac in hypoxia treated lenses increased while levels of repressive modifications H3K9me3 and H3K27me3 remained unchanged. Hypoxia-specific H3K4me3 and/or H3K27ac regions were detected within 5 kb of the transcriptional start sites of over 900 fiber cell genes with increased expression upon hypoxia exposure and 350 genes with decreased expression. Inhibition of histone writers and erasers resulted in altered levels of key fiber cell genes upon hypoxia exposure. The results provide evidence that hypoxia induced histone modifications regulate genes required for mature lens formation and they provide a framework for understanding the role of hypoxia specific histone modifications in the regulation of genes in more complex tissues.

2025-12-02 | GSE309107 | GEO

Nguyen2013 - Dynamic model of HIF regulation in hypoxia

Project description: Not available

| MODEL1912100004 | biostudies-other

Hypoxia-driven histone modifications govern gene regulation for mature eye lens formation [CUT&Run]

2025-12-02 | GSE309116 | GEO

Tumor Suppressor IKZF1 Mediates Glucocorticoid Therapy Resistance in B Cell Precursor Acute Lymphoblastic Leukemia

Project description:Analysis of the effect of Prednisolone in mouse splenocytes with and without Ikzf1 at gene expression level. The hypothesis tested in the present study was that loss of Ikzf1 affects the induction and repression of the Glucocorticoid receptor target genes. Results provide important information of the differentially expressed genes regulated by Ikzf1 upon Prednisolone treatment, explaining the resistance towards Glucocorticoid-induced apoptosis in splenocytes harboring Ikzf1 loss.

2015-02-04 | GSE65554 | GEO

Hypoxia promotes stem cell phenotypes and poor prognosis through epigenetic regulation of DICER [HMLER]

Project description:MicroRNAs are small regulatory RNAs that post-transcriptionally control gene expression. Reduced expression of DICER, the enzyme involved in microRNA processing, is frequently observed in cancer and is associated with poor clinical outcome in various malignancies. Yet the underlying mechanisms are not well understood. Here, we identify tumor hypoxia as a regulator of DICER expression in large cohorts of breast cancer patients. We show that DICER expression is suppressed by hypoxia through an epigenetic mechanism that involves inhibition of oxygen-dependent H3K27me3 demethylases KDM6A/B and results in silencing of the DICER promoter. Subsequently, reduced miRNA processing leads to derepression of the miR-200 target ZEB1, stimulates the epithelial to mesenchymal transition and ultimately results in the acquisition of stem cell phenotypes in human mammary epithelial cells. Our study uncovers a previously unknown relationship between oxygen-sensitive epigenetic regulators, miRNA biogenesis and tumor stem cell phenotypes that may underlie poor outcome in breast cancer. A total of 12 samples were analyzed. For each condition tested, 3 independent experiments were carried out (biological repicates).

2014-09-30 | E-GEOD-61721 | biostudies-arrayexpress

Hypoxia-induced metabolic dysfunction in WAT

Project description:Background: Excessive white adipose tissue (WAT) expansion as in obesity is generally associated with chronic inflammation of WAT, which contributes to obesity associated complications. Low oxygen availability in WAT is hypothesized to be the initiator of this inflammatory response. Hypothesis: We examined the hypothesis that local tissue hypoxia is responsible for the initiation of inflammation in WAT. Research design and methods: Diet-induced obese male C57BL/6JOlaHsd mice, housed at thermoneutrality, were exposed to mild environmental oxygen restriction (OxR, to 13% oxygen) for five days and compared with mice kept at normoxia, after which WAT and serum were collected. Body composition, systemic metabolic parameters, WAT macrophage infiltration (as marker for tissue inflammation) and whole genome microarray analysis, and circulating adipokines were measured. Results: Five days OxR decreased body weight and fat mass, and increased blood levels of haemoglobin and haematocrit, as well as lactate to glucose ratio, which indicated systemic hypoxia. No difference in adipose tissue inflammation was found, which was supported by down regulation of inflammation-associated transcript levels of S100a8, Saa1, and Saa3. Serum metabolomics revealed an increase of branched chain amino acid Valine and propionylcarnitine. Adipokines CCDC3, CCK, and Adiponectin are reduced by OxR on transcript (Cck) or serum protein level (Adiponectin), or both (CCDC3). Conclusions: Mild oxygen restriction does not increase white adipose tissue inflammation in obese mice. However, a systemic adaptation together with a metabolic response in WAT was observed.

2019-06-24 | GSE53802 | GEO

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