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Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated chronically with ovalbumin

ABSTRACT: Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated chronically with ovalbumin

PROVIDER: PRJNA754101 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15425200_1.fastq.gz	Fastqsanger.gz
	SRR15425200_2.fastq.gz	Fastqsanger.gz
	SRR15425201_1.fastq.gz	Fastqsanger.gz
	SRR15425201_2.fastq.gz	Fastqsanger.gz
	SRR15425202_1.fastq.gz	Fastqsanger.gz

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Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated chronically with ovalbumin

Project description:Background: HAS2 is a member of the gene family encoding hyaluronan synthase 2 (HAS2), which can generate high-molecular-weight hyaluronan (HMW-HA). Our previous study identified HAS2 as a candidate gene for susceptibility to adult asthma. However, little is known if HAS2 dysfunction affects airway remodeling and steroid insensivity. In this study, we clarified the dysfunction of Has2 triggering severe airway remodeling and steroid insensitivity in a murine model of asthma. Methods: Ovalbumin (OVA) was used to induce eosinophilic airway inflammation and airway remodeling in Has2 heterozygous deficient (Has2+/−) mice and their wild-type (WT) littermates. Lung tissue histology, bronchoalveolar lavage fluid cell counting, quantitative PCR, HA size analysis, multiplex cytokines and chemokines analysis, RNA sequencing, anti IL-17 neutralization experiment were performed. Results: After chronic OVA stimulation, Has2+/− (Has2+/--OVA) mice showed significant decrease of Has2 mRNA expression levels, HMW-HA, HA-binding protein, and TGF-β. Has2+/--OVA mice demonstrated increased eosinophilic airway inflammation, goblet cell hyperplasia, and IL-17 levels. RNA sequencing demonstrated downregulation of EIF2 signaling pathways, TGF-β signaling pathways, and heat shock proteins with Th17 bias in Has2+/--OVA mice. Combined treatment with anti IL-17 antibody and dexamethasone reduce steroid insensitivity in Has2+/--OVA mice Conclusions: Has2 attenuation worsen eosinophilic airway inflammation, airway remodeling, and steroid insensitivity. This severe intractable phenotype might be induced by impairment of TGF-β signaling and ER stress response related signaling. These data highlight that HAS2 and HMW-HA are important for controlling intractable eosinophilic airway inflammation and remodeling, and could potentially be exploited for therapeutic benefit to asthma patients.

2022-01-26 | GSE181966 | GEO

Gene signature profiles in lung tisses of wild type mice or Has2 heterozygous deficient mice stimulated with ovalbumin

Project description:Background: HAS2 is a member of the gene family encoding hyaluronan synthase 2 (HAS2) which can generate high molecular weight hyaluronan (HMW-HA). Although we previously reported that HAS2 is a novel candidate gene for susceptibility to adult asthma., little is known about whether HAS2 dysfunction affect eosinophilic airway inflammation. Objective: We therefore hypothesized that attenuation of HAS2 will enhance eosinophilic airway inflammation. Methods: C57BL/6 wild type (WT) mice, Has2 heterozygous deficient (Has2+/−) mice were used in eosinophilic airway inflammation model which induced by ovalbumin (OVA). Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed to detect Has2 and HA binding protein mRNA expression levels. Lung tissue and lavage fluid (BALF) were analyzed for inflammation and various cytokines and chemokines. Airway resistance was measured using forced oscillation technique. gene expression analyses were also performed to elucidate further pathogenesis. Results: The expression levels of Has2 mRNA was significantly decreased in OVA stimulated Has2+/− (Has2+/−-OVA) mice. Has2+/−-OVA mice also displayed significant reduce of CD44, and TGF-beta1 mRNA expression. BALF eosinophil number, levels of various Th2 cytokines and chemokines in BALF, and airway responsiveness were significantly increased in Has2+/−-OVA mice compared with similarly treated WT mice. ILK Signaling and PKA signaling were downregulated significantly more in Has2+/−-OVA mice compared with similarly treated WT mice. Conclusions: Has2 dysfunction induce more intense allergic eosinophilic airway inflammation and increase of airway hyper responsiveness with impairment of HAS2-CD44-TGF-beta signaling. Modulating HAS2 signaling might provide novel therapeutic targets for intractable bronchial asthma patients.

2022-04-04 | GSE148161 | GEO

Gene signature profiles in lung tisses of wild type mice or Has2 heterozygous deficient mice stimulated with ovalbumin

Project description:Gene signature profiles in lung tisses of wild type mice or Has2 heterozygous deficient mice stimulated with ovalbumin

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Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated with porcine pancreatic elastase

Project description:Chronic obstructive pulmonary disease (COPD) is an inflammatory lung condition primarily caused by prolonged exposure to harmful substances, such as cigarette smoke. Hyaluronic acid synthase 2 (HAS2) synthesizes high-molecular-weight hyaluronic acid (HMW-HA), believed to have anti-inflammatory properties. Previous studies have suggested that HAS2 dysfunction may exacerbate COPD. However, the specific impact of HAS2 on pulmonary emphysema progression remains unclear. In this study, we tested the hypothesis that HAS2 dysfunction worsens airway inflammation and emphysema in mouse COPD model. Has2 heterozygous-deficient (Has2+/-) mice and their wild-type (WT) littermates have been evaluated in a porcine pancreatic elastase (PPE)-induced COPD model. Following PPE administration, Has2+/- mice exhibited a significant increase in total cell and neutrophil counts in BALF samples compared to WT mice. Has2+/- mice demonstrated enhanced emphysema development on histological analyses, with higher values of mean linear intercept relative to wild-type mice. Elastase-stimulated Has2+/- mice also demonstrated increased G-CSF level and TGF-β attenuation in lung. RNA-seq analysis suggested that PPE stimulation promotes HMW-HA synthesis and TGF-β signaling. GO analysis using Has2+/- mice-specific DEGs showed that genes associated with pathways that "negative regulation of transforming growth factor beta receptor signaling pathway" were activated after PPE administration. This study demonstrates that Has2 dysfunction exacerbates neutrophilic airway inflammation and emphysema, underscoring the protective role of HAS2 in a PPE induced emphysema model. The exacerbated response appears to involve G-CSF and TGF-β-related signaling pathways. These findings may contribute to the development of novel therapeutic strategies for COPD management.

2025-09-26 | GSE304417 | GEO

Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated with porcine pancreatic elastase

Project description:Gene signature profiles in lung tissues of wild type mice or Has2 heterozygous deficient mice stimulated with porcine pancreatic elastase

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UCP exposure of ovalbumin sensitized and challenged mice

Project description:UCP exposure of ovalbumin sensitized and challenged mice

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Hyaluronic Acid Synthase-2 (HAS2) overexpression and deficiency effect on hepatic stellate cells

Project description:Analysis of hepatic stellate cells (HSCs) isoltaed from ASMA-HAS2 transgenic and HSC-specific Has2 knockout mice. HAS2 synthesized hyaluronic acid, one of major extracellular matrix. Results provide insight into the role of HAS2 in hepatic stellate cells.

2020-01-01 | GSE108593 | GEO

UCP exposure of ovalbumin sensitized and challenged mice

Project description:To gain insight into the promoting effect of ultrafine particle inhalation on development and progression of allergic asthma, we selected an experimental approach involving exposure to ultrafine carbon particles (UCP) and gene expression profiling of lungs from mice with experimental, ovalbumin induced allergy. Comparative gene expression analysis was performed by hybridizing pooled cDNA samples from lavaged lungs of different groups. The results suggest that allergic sensitization may represent an susceptibility factor for effects of UCP on gene expression in the lung. In sensitized individuals UCP exposure, such as found in polluted air, thus may contribute to the development and/or aggrevation of allergic asthma. Keywords: Particle Inhalation, lung, ovalbumin sensitized and challanged, expression profling

2007-07-01 | GSE6571 | GEO

Celecoxib, Rofecoxib Chronically Treated Mice, Aorta RNA-Seq

Project description:Celecoxib, Rofecoxib Chronically Treated Mice, Aorta RNA-Seq

2020-03-07 | GSE95802 | GEO