Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA308084 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:To determine the GATA3 or HIF-1α regulated gene expression profile in OEC-M1 cells under hypoxia
2017-06-30 | GSE76581 | GEO
Project description:Analysis of Huh-7 hepatocarcinoma cell line depleted of NDRG3 or HIF-1α under hypoxic condition. HIF-1α and NDRG3 have distinct functions in hypoxia responses. Results provide insight into molecular basis of HIF-independent signaling in the development and progression of hypoxic tumors Gene expression profiles of Huh-7 cells stably expressing NDRG3-shRNA or HIF-1α-shRNA under normoxia were compared to gene expression profiles of Huh-7 stable cells under hypoxia for 6, 12 and 24 hours.
2015-07-24 | E-GEOD-55212 | biostudies-arrayexpress
Project description:Analysis of Huh-7 hepatocarcinoma cell line depleted of NDRG3 or HIF-1α under hypoxic condition. HIF-1α and NDRG3 have distinct functions in hypoxia responses. Results provide insight into molecular basis of HIF-independent signaling in the development and progression of hypoxic tumors Gene expression profiles of Huh-7 cells stably expressing NDRG3-shRNA or HIF-1α-shRNA under normoxia were compared to gene expression profiles of Huh-7 stable cells under hypoxia for 3, 6, 12 and 24 hours.
2015-07-24 | E-GEOD-59729 | biostudies-arrayexpress
Project description:Hypoxia-inducible factor 1 (HIF-1) is a transcriptional regulator that mediates cellular adaptive responses to hypoxia. Hypoxia-inducible factor 1α (HIF-1α) is involved in the development of ascites syndrome (AS) in broiler chickens. Therefore, studying the effect of HIF-1α on the cellular transcriptome under hypoxic conditions will help to better understand the mechanism of HIF-1α in the development of AS in broilers. In this study, we analyzed the gene expression profile of the DF-1 cell line under hypoxic conditions by RNA-seq. Additionally, we constructed the HIF-1α knockdown DF-1 cell line by using the RNAi method and analyzed the gene expression profile under hypoxic conditions. The results showed that exposure to hypoxia for 48 hours had a significant impact on the expression of genes in the DF-1 cell line, which related to cell proliferation, stress response, and apoptosis. In addition, after HIF-1α knockdown more differential expression genes appeared than in wild-type cells, and the expression of most hypoxia-related genes was either down-regulated or remained unchanged. Pathway analysis results showed that differentially expressed genes were mainly enriched in pathways related to cell proliferation, apoptosis, and oxidative phosphorylation. Our study obtained transcriptomic data from chicken fibroblasts at different hypoxic times and identified the potential regulatory network associated with HIF-1α. This data provides valuable support for understanding the transcriptional regulatory mechanism of HIF-1α in the development of AS in broilers.
2023-11-15 | GSE244260 | GEO
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
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 | GSE269141 | GEO
Project description:Transcription mediated by hypoxia inducible factor (HIF-1) contributes to tumor angiogenesis and metastasis but is also involved in the activation of cell-death pathways and normal physiological processes. Given the complexity of HIF-1 signaling it could be advantageous to target a subset of HIF-1 effectors rather than the entire pathway. We compared the genome-wide effects of three molecules that each interfere with the HIF-1-DNA interaction: a polyamide targeted to the hypoxia response element (HRE), siRNA targeted to HIF-1α, and echinomycin, a DNA binding natural product with a similar but less specific sequence preference to the polyamide. The polyamide affects a subset of hypoxia-induced genes that are consistent with the binding site preferences of the polyamide. For comparison, siRNA targeted to HIF-1α and echinomycin each affect the expression of nearly every gene induced by hypoxia. Remarkably, the total number of genes affected by either polyamide or HIF-1α siRNA over a range of thresholds is comparable. The data shows how polyamides can be used to affect a subset of a pathway regulated by a transcription factor. In addition, this study offers a unique comparison of three complementary approaches towards exogenous control of endogenous gene expression. Experiment Overall Design: Hypoxia-mimetic DFO (deferoxamine)-stimulated U251 cells that were treated with polyamide 1, HIF-1α siRNA, and echinomycin were compared to control cells that were also DFO-stimulated. Cells not stimulated with DFO were also compared to the DFO-stimulated controls. Three biological replicates were included for each treatment/condition.
2008-06-15 | E-GEOD-7835 | biostudies-arrayexpress
Project description:The adaptive responses to oxygen depletion orchestrated by hypoxia-inducible factors (HIFs) produce profound effects on multiple pathways. A canonical metabolic response is enhanced fermentation, but this can generate an unfavorably acidic environment under poor capillary perfusion. It is unclear how cells balance the metabolic benefits of hypoxic responses against knock-on consequences on acid-base homeostasis. We studied the interplay between hypoxia and acidosis on HIF signaling in colorectal cancer cell lines that can survive acidic conditions. Hypoxia stabilized HIF-1α, but this effect was transient in combination with acidosis. By 48 h, HIF-1α induction decreased in proportion to acidification. Proteomic analyses identified responses that followed HIF-1α, including canonical HIF targets (CA9, PDK1), but these did not reflect a proteome-wide downregulation. Responses to acidosis and hypoxia were enriched in lysosomal proteins, but not proteasomal components, implicating the former degradation pathway in transient HIF-1α activation under acidosis. Moreover, HIF-1α decay was not due to decreased HIF1A transcription but was blocked by lysosomal inactivation (bafilomycin-A1). Acidotic hypoxia increased the abundance of lysosomes and activated autophagy by disabling the inhibitory influence of mammalian target of rapamycin complex 1, resulting in HIF-1α degradation. By blocking HIF-driven fermentative upregulation, this mechanism protects the cellular environment from deleterious acid-overloading, an outcome that outweighs the biosynthetic benefits of raised glycolytic flux under suppressed respiration. Thus, alkaline conditions are permissive for at least some aspects of HIF-1α signaling, but may not reflect tumor microenvironment chemistry. Consequently, acidic hypoxic tumor regions may not necessarily overlay with sites of HIF induction
2025-06-30 | PXD062474 | Pride
Project description:Hypoxia can be established under pathological conditions, such as cancer, due to the imbalance between oxygen supply and consumption. Hypoxia Inducible Transcription Factor HIF-1 mediates the physiological response to hypoxia but also regulates multiple steps of carcinogenesis. Despite its well-defined oxygen-dependent activation, many aspects of HIF-1 transcriptional activity as well as interaction with chromatin remain elusive. We have recently shown that TFAP2A physically interacts with HIF-1 and hypoxia-dependent deSUMOylation of TFAP2A positively affects HIF-1 activity. We now present ChIP-seq analysis showing that TFAP2A resides together with HIF-1α on the promoters of a subset of hypoxia-regulated genes, the mRNA expression of which is downregulated by silencing of TFAP2A. Interestingly, CRISPR-mediated knockdown of TFAP2A expression under hypoxia decreased the occupancy of HIF-1α on these promoters and affected chromatin accessibility. Mechanistically, we reveal that the Ku70/Ku80 protein complex interacts with TFAP2A in a SUMO-dependent manner under hypoxia and participates in HIF-dependent gene expression. Moreover, using stable expression of TFAP2A forms that either lack or constitutively carry a SUMO modification, we could show that SUMOylation affects binding of TFAP2A to chromatin. Overall, our data suggest that TFAP2A is an important co-regulator of the HIF-1-dependent transcriptional response to hypoxia and SUMOylation fine-tunes this regulation. As both TFAP2A and HIF-1 play critical roles in cancer progression, a detailed characterization of their crosstalk could lead to novel therapeutic strategies for targeting and killing cancer cells in hypoxic tumors.
2025-05-23 | PXD053747 | Pride
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