Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Intestine epithelial specific hypoxia-inducible factor-1α overexpression on ileum transcriptome

ABSTRACT: Intestine epithelial specific hypoxia-inducible factor-1α overexpression on ileum transcriptome

PROVIDER: PRJNA1177978 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR31125108_1.fastq.gz	Fastqsanger.gz
	SRR31125108_2.fastq.gz	Fastqsanger.gz
	SRR31125109_1.fastq.gz	Fastqsanger.gz
	SRR31125109_2.fastq.gz	Fastqsanger.gz
	SRR31125110_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 12

Similar Datasets

Intestine epithelial specific hypoxia-inducible factor-1α overexpression on ileum transcriptome

Project description:Background: Intestine epithelial hypoxia-inducible factor-1α (HIF-1α) plays a critical role in maintaining gut barrier function. The aim of this study was to determine genetic activation of intestinal HIF-1α ameliorates western diet-induced metabolic dysfunction–associated steatotic liver disease (MASLD). Methods: Male and/or female intestinal epithelial-specific Hif1α overexpression mice (Hif1α LSL/LSL;VilERcre) and wild-type littermates (Hif1α LSL/LSL) were fed with regular chow diet, high fructose (HFr) or high-fat (60% Kcal) high-fructose diet (HFHFr) for 8 weeks. Metabolic phenotypes were profiled. Results: Male Hif1α LSL/LSL;VilERcre mice exhibited markedly improved glucose tolerance compared to Hif1α LSL/LSL mice in response to HFr diet. Eight weeks HFHFr feeding led to obesity in both Hif1α LSL/LSL;VilERcre and Hif1α LSL/LSL mice. However, male Hif1α LSL/LSL;VilERcre mice exhibited markedly attenuated hepatic steatosis along with reduced liver size and liver weight compared to male Hif1α LSL/LSL mice. Moreover, HFHFr-induced systemic inflammatory responses were mitigated in male Hif1α LSL/LSL;VilERcre mice compared to male Hif1α LSL/LSL mice and those responses were not evident in female mice. Ileum RNA-seq analysis revealed that glycolysis/gluconeogenesis was up in male Hif1α LSL/LSL;VilERcre mice accompanied by increased epithelial cell proliferation. Conclusion: Our data provide evidence that genetic activation of intestinal HIF-1α markedly ameliorates western diet-induced MASLD in a sex-dependent manner. The underlying mechanism is likely attributed to HIF-1α activation induced upregulation of glycolysis, which, in turn, leading to enhanced epithelial cell proliferation and augmented gut barrier function.

2024-10-26 | GSE280362 | GEO

Hypoxia-inducible Factor 1α Mediated Lactylation to Enhance Inflammatory Response during Hypoxia induced lung dysfunction

Project description:Hypoxia can result in tissue dysfunction, metabolic alterations, and structural damage within the pulmonary tissue, thereby impacting lung ventilation and air exchange. The identification of Hypoxia-inducible factor (Hif) 1α as a pivotal mediator in the inflammatory cascade subsequent to hypoxia induction has been established. However, the mechanism remains elusive. To delve deeper into this phenomenon, we have developed a murine model of sustained hypoxia and utilized nanocarriers for the delivery of lentivirus Hif-1α for knockdown purposes. Our findings suggest that under conditions of sustained hypoxia, knockdown of Hif-1α effectively ameliorated SpO2 levels and attenuated lung injury in our murine model. We observed that Hif-1α-mediated Histone Lactylation was evident in the lungs exposed to sustained hypoxia. Through RNA-seq and ChIP-seq profiling, we determined that upregulation of Hif-1α expression in sustained hypoxic lung tissue is essential for inducing lactylation enrichment of inflammatory response genes. Furthermore, knockdown of Hif-1α returned to normal inflammatory cytokines (e.g. TNF-α, IL-6 and IL-1β). Analysis of plasma metabolites from individuals experiencing restrictive/ obstructive lung disease revealed a significant enrichment of the Warburg effect within the sustained hypoxic group. Thus, our study provides compelling evidence supporting the notion that targeting Hif-1α-mediated histone lactylation may represent a promising therapeutic strategy for managing sustained hypoxia-induced lung injury.

2025-06-12 | GSE269142 | GEO

Hypoxia Inducible Factor 1α-driven steroidogenesis impacts systemic hematopoiesis

Project description:Hypoxia Inducible Factor 1α-driven steroidogenesis impacts systemic hematopoiesis

| PRJNA1241793 | ENA

Hypoxia-inducible Factor 1α Mediated Lactylation to Enhance Inflammatory Response during Hypoxia induced lung dysfunction [RNA-seq]

2025-06-12 | GSE269141 | GEO

Expression data from ileum of inducible intestine-specific GATA6 knockout mice

2011-06-07 | GSE22416 | GEO

Hypoxia-inducible Factor 1α Mediated Lactylation to Enhance Inflammatory Response during Hypoxia induced lung dysfunction

Project description:Hypoxia-inducible Factor 1α Mediated Lactylation to Enhance Inflammatory Response during Hypoxia induced lung dysfunction

| PRJNA1120396 | ENA

Activating injury-responsive genes with hypoxia enhances axon regeneration through neuronal HIF-1α

Project description:Injured peripheral neurons successfully activate a pro-regenerative transcriptional program to enable axon regeneration and functional recovery. How transcriptional regulators coordinate the expression of such programs remains unclear. Here we show that hypoxia-inducible factor 1α (HIF-1α) controls multiple injury-induced genes in sensory neurons and contribute to the pre-conditioning lesion effect. Knockdown of HIF-1α in vitro or conditional knockout in vivo impairs sensory axon regeneration. The HIF-1α target gene Vascular Endothelial Growth Factor A (VEGFA) is expressed in injured neurons and contributes to stimulate axon regeneration. Induction of HIF-1α using hypoxia enhances axon regeneration in vitro and in vivo in sensory neurons. Hypoxia also stimulates motor neuron regeneration and accelerates neuromuscular junction reinnervation. This study demonstrates that HIF-1α represents a critical transcriptional regulator in regenerating neurons and suggests hypoxia as a tool to stimulate axon regeneration.

2016-01-21 | GSE73415 | GEO

Hypoxia-inducible factor-1α promotes cell survival during ammonia stress response in ovarian cancer stem-like cells

Project description:Ammonia is a toxic by-product of metabolism that causes cellular stress. Although a number of proteins are involved in adaptive stress response, specific factors that counteract ammonia-induced cellular stress and regulate cell metabolism that facilitate survival against toxicity have yet to be identified. We demonstrated that hypoxia-inducible factor-1α (HIF-1α) is stabilised and activated by ammonia stress. HIF-1α activated by ammonium chloride compromises ammonia-induced apoptosis. Furthermore, we identified glutamine synthetase (GS) as a key driver of cancer cell proliferation and glutamine-dependent metabolism under ammonia stress in ovarian cancer stem-like cells expressing CD90. Interestingly, activated HIF-1α counteracts glutamine synthetase function in glutamine metabolism by facilitating glycolysis and elevating glucose dependency. Our studies reveal the hitherto unknown functions of HIF-1α in biphasic ammonia stress management in cancer stem-like cells. GS facilitates proliferation and HIF-1α contributes to metabolic remodelling in cellular energy usage resulting in attenuated proliferation but conversely promoting cell survival.

2017-11-22 | GSE107251 | GEO

Transcriptome analysis using Quant-RNAseq after NPM1 or HIF-1α silencing under normoxia or Hypoxia

Project description:Hypoxia inducible factor-1 (HIF-1) is a central transcriptional regulator of genes associated with adaptive responses to hypoxia. NPM1 is a histone chaperone found to associate with HIF-1α in a phosphorylation dependent manner and increase its activty. The aim of this study was to find if HIF-1α and NPM1 regualate gene expression under hypoxia. Transcriptome analysis using Quant-RNA-seq after HIF-1α or NPM1 silencing under hypoxia reveals a significant number of genes, the hypoxic expression of which depends on both proteins.

2021-12-15 | GSE158890 | GEO

Expression data from ileum of inducible intestine-specific GATA6 knockout mice

Project description:GATA6 is a transcription factor involved in the differentiation of intestinal epithelial cells into differentiated absorptive epithelial cells. GATA6 is expressed in all segments of the small intestine. We examined the impact of deleting GATA6 from intestinal epithelial cells of the adult ileum 6-8 week old Villin-CreERT2 mice or Villin-CreERT2 mice crossed to GATA6 flox/flox mice were treated with a single injection of tamoxifen. (100 mg/ml) for 5 consecutive days. 28 days later the ileum was dissected and RNA prepared from the whole ileal segment using the RNAeasy method with DNAse treatment. Three individual mice were examined in each of the control and GATA6 KO groups.

2011-06-07 | E-GEOD-22416 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data