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Hypoxic response for human bronchial epithelial culture [bulkRNA-Seq batch1]

ABSTRACT: Purpose: To identify the gene expression change under hypoxia on HBE cells. Methods: bulk RNA-seq was performed on primary human bronchial epithelial cells (HBE) that were cultured on air-liquid interface (ALI) condition and treated under normoxia or hypoxia (1% O2) for 6hr, 24hr, and 5days. Results: hypoxia-related genes were significantly upregulated under hypoxia including EGLN3.

ORGANISM(S): Homo sapiens

PROVIDER: GSE227502 | GEO | 2023/08/22

REPOSITORIES: GEO

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Chronic hypoxic response for human bronchial epithelial culture [bulkRNA-Seq batch2]

Project description:Purpose: To identify the gene expression change under chronic hypoxia on HBE cells. Methods: bulk RNA-seq was performed on primary human bronchial epithelial cells (HBE) that were cultured on air-liquid interface (ALI) condition and treated under normoxia or hypoxia (1% O2) for 5days. Results: inflammatory cytokines, collagen degradation, and angiogenic genes were upregulated under chronic hypoxia.

2023-08-22 | GSE227501 | GEO

Cellular response to hypoxia on human bronchial epithelial culture [scRNA-Seq]

Project description:Purpose: To identify the cell types change and gene expression change under hypoxia on HBE cells. Methods: The primary human bronchial epithelial cells (HBE) were cultured on air-liquid interface (ALI) conditions. After 4 weeks, the cells were cultured under normoxic or hypoxic (1% O2) conditions for 6h or 5days. The cells were dissociated with Accutase solution and proceeded to scRNA-seq. Results: Hypoxia did not induce any hypoxia-specific cell types, however, all cell types upregulated hypoxia-related, and senescence-related genes and downregulated cell proliferation genes.

2023-08-22 | GSE227508 | GEO

Cellular response to hypoxia on human bronchial epithelial culture [scRNA-Seq CAP]

Project description:Purpose: To identify the cell types change and gene expression change under hypoxia on HBE cells. Methods: The primary human bronchial epithelial cells (HBE) were cultured on air-liquid interface (ALI) conditions. After 4 weeks, the cells were cultured under normoxic, symmetrical hypoxic (3.5% O2), or asymmetrical hypoxic (3.5% O2 basolateral with apical cap ~ 1% O2) conditions for 5 days. The cells were dissociated with Accutase solution and proceeded to scRNA-seq. Results: Asymmetrical hypoxic cells showed more hypoxia-related responses than symmetrical hypoxic cells.

2023-08-22 | GSE227586 | GEO

Open chromatin and transcriptome analysis of iPSCs differentiated into lung epithelium at air-liquid interface reveals key transcriptional drivers and processes (RNA-seq data)

Project description:The availability of robust protocols to differentiate induced pluripotent stem cells (iPSCs) into many human cell lineages has transformed research into the origins of human disease. The efficacy of differentiating iPSCs into specific cellular models is influenced by many factors including both intrinsic and extrinsic features. Among the most challenging models is the generation of human bronchial epithelium at air-liquid interface (HBE-ALI), which is the gold standard for many studies of respiratory diseases including cystic fibrosis. Here we perform open chromatin mapping by ATAC-seq and transcriptomics by RNA-seq in parallel, to define the functional genomics of key stages of the iPSC to HBE-ALI differentiation. Within open chromatin peaks the overrepresented motifs include the architectural protein CTCF at all stages, while motifs for the FOXA and GATA pioneer factors families are only seen at early stages, and those regulating key airway epithelial functions, such as EHF, are limited to later stages. The RNA-seq data illustrate dynamic pathways during the iPSC to HBE-ALI differentiation, and also the marked functional divergence of different iPSC lines at the ALI stages of differentiation. Moreover, a comparison of iPSC-derived and lung donor-derived HBE-ALI cultures reveals substantial differences between these models.

2021-01-06 | GSE136858 | GEO

Novel data integration approaches identify concordant and discordant immune responses between mice and humans [human cells]

Project description:We have conducted experiments to compare transcriptional response to tuberculosis (TB) in THP1 cells in time points 1hr,6hr and 24hr after infection.

2017-09-21 | GSE89391 | GEO

RNA-seq 6 day timecourse for K562 cells grown in hypoxia/normoxia (21%, 5%, 1% oxygen)

Project description:K562 cells were grown at different oxygen levels (21%, 5%, 1%) and samples were collected at 6hr, 24hr, 3day, and 6day time points (triplicate per time point).

2020-01-31 | GSE144527 | GEO

Open chromatin and transcriptome analysis of iPSCs differentiated into lung epithelium at air-liquid interface reveals key transcriptional drivers and processes (ATAC-seq data)

Project description:The availability of robust protocols to differentiate induced pluripotent stem cells (iPSCs) into many human cell lineages has transformed research into the origins of human disease. The efficacy of differentiating iPSCs into specific cellular models is influenced by many factors including both intrinsic and extrinsic features. Among the most challenging models is the generation of human bronchial epithelium at air-liquid interface (HBE-ALI), which is the gold standard for many studies of respiratory diseases including cystic fibrosis. Here we perform open chromatin mapping by ATAC-seq and transcriptomics by RNA-seq in parallel, to define the functional genomics of key stages of the definitive endoderm (DE) to HBE-ALI differentiation. Within open chromatin peaks the overrepresented motifs include the architectural protein CTCF at all stages, while motifs for the FOXA and GATA pioneer factors families are only seen at early stages, and those regulating key airway epithelial functions such as EHF are limited to later stages. The RNA seq data illustrate dynamic pathways during the DE to HBE-ALI differentiation and also the marked functional divergence of different iPSC lines at the ALI stages of differentiation. Moreover, a comparison of iPSC-derived and lung donor-derived HBE cultures reveals substantial differences in these culture models.

2021-01-06 | GSE136857 | GEO

Identification of differential signaling cues in insulin/IGF1 signaling pathways in breast cancer

Project description:Temproral networks of (phospho)-proteins are constructed and analyzed to infer differential interactions under insulin and IGF1 stimulation. In total, 134 antibodies are tested in 21 breast cancer cell lines. The experiments are done in triplicate. Three serum-free-condition time points (5min, 24hr, 48hr) and six stimulation time points (5min, 10min, 30min, 6hr, 24hr, and 48hr) are obtained with either 10 nM IGF1 or 10 nM insulin stimulation.

2016-07-21 | E-GEOD-80233 | biostudies-arrayexpress

The inhibitory effect of EGLN3 on proliferation in gastric cancer cells

Project description:Background: Egl-9 family hypoxia inducible factor 3 (EGLN3) belongs to the family of 2-oxoglutarate (2-OG)- and ferrous iron (Fe 2+)-dependent dioxygenases, which play critical roles in all steps of tumorigenesis. Previous studies have found that EGLN3 regulates the malignant biological behavior of malignant tumors. However, its role and mechanism in the occurrence and development of gastric cancer (GC) are still unclear. This study aimed to investigate the role of EGLN3 in gastric carcinogenesis Methods:Bioinformatics analysis, qRT-PCR, western blot, CCK-8, and in vivo xenograft tumor model were used to examine the expression and function of EGLN3. Survival analysis was performed to determine the correlation between EGLN3 expression and prognosis of patients with GC. Genes modulated by EGLN3 in NCI-N87 cells were identified through RNA next generation sequence screening and further verified by qRT-PCR in NCI-N87 cells. Results: EGLN3 expression was markedly reduced in GC tissues as compared with that in normal tissues. Likewise, EGLN3 expression was also significantly reduced in a panel of GC cell lines . Forced expression of EGLN3 inhibited proliferation in NCI-N87 cells in vitro. Additionally, EGLN3 impaired growth of NCI-N87 cells in immunodeficient mice. Survival analysis showed that EGLN3 expression was positively associated with favorable outcome in patients with GC.

2024-04-12 | GSE200646 | GEO

Expression data from the cells of rat bronchoalveolar lavage fluid

Project description:Acute lung injury (ALI) refers to a clinical syndrome characterized by bilateral lung injury, severe lung diffuse failure and hypoxemia caused by non-cardiogenic pulmonary edema.Sepsis is the leading etiology of ALI and a common admission to the intensive care unit, which induces pulmonary inflammation leading disruption of endothelial-epithelial barriers by surge release of pro-inflammatory cytokines that increases the permeability of the alveolar-capillary membrane, pulmonary infiltration, and edema.Ultimately, gas exchange across the alveolar-capillary membrane is severely impaired and acute respiratory failure and hypoxia occur. ALI patients may suffer from pulmonary inflammation and hypoxia simultaneously or sequentially, those two pathophysiological processes may interact mutually and contribute together to the development of ALI. LPS is the most important biological mediator of sepsis induce secretion of inflammatory cytokines including TNF-α, IL-1, and IL-6 from many cell types in response to bacterial toxins. Thus LPS has been commonly used to establish inflammatory ALI models of rats and mice. Clinically, hypoxia commonly coexists with sepsis; however, the role of hypoxia on the development of inflammatory ALI is unclear. The understanding of interaction of hypoxia and inflammation in ALI is of the importance for the treatment of ALI.

2018-08-21 | GSE111241 | GEO

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