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Myeloid Zfhx3 Deficiency Protects Against Hypercapnia-induced Suppression of Host Defense Against Influenza A Virus

ABSTRACT: Myeloid Zfhx3 Deficiency Protects Against Hypercapnia-induced Suppression of Host Defense Against Influenza A Virus

PROVIDER: PRJNA762340 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15844682.fastq.gz	Fastqsanger.gz
	SRR15844683.fastq.gz	Fastqsanger.gz
	SRR15844684.fastq.gz	Fastqsanger.gz
	SRR15844685.fastq.gz	Fastqsanger.gz
	SRR15844686.fastq.gz	Fastqsanger.gz

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Myeloid Zfhx3 Deficiency Protects Against Hypercapnia-induced Suppression of Host Defense Against Influenza A Virus

Project description:Zfhx3, human ortholog of the Drosophila Zfh2 and first known mediator of hypercapnic immune suppression in vivo, is expressed in human and mouse MØs and its myeloid deletion reversed the effects of hypercapnia in gene expression in murine alveolar macrophages and protects against influenza A virus proliferation, lung injury and mortality increased by hypercapnia in infected mice.

2024-01-21 | GSE183922 | GEO

Myeloid Zfhx3 Deficiency Protects Against Influenza A Virus-induced Lung Injury and Mortality Increased by Hypercapnia

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Myeloid Zfhx3 Deficiency Protects Against Influenza A Virus-induced Lung Injury and Mortality Increased by Hypercapnia

Project description:Myeloid Zfhx3 Deficiency Protects Against Influenza A Virus-induced Lung Injury and Mortality Increased by Hypercapnia

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Myeloid Zfhx3 deficiency protects against hypercapnia-induced suppression of host defense against influenza A virus.

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Toll-Like-Receptor 5 Reduces Lung Dysbiosis and Protects Against Pulmonary Fibrosis

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Hypercapnia Alters Expression of Immune Response, Nucleosome Assembly and Lipid Metabolism Genes in Differentiated Human Bronchial Epithelial Cells

Project description:Hypercapnia, the elevation of CO2 in blood and tissues, commonly occurs in severe acute and chronic respiratory diseases, and is associated with increased risk of mortality. Recent studies have shown that hypercapnia adversely affects innate immunity, host defense, lung edema clearance, and cell proliferation. Airway epithelial dysfunction is a feature of advanced lung disease, but the effect of hypercapnia on airway epithelium is unknown. Thus, in the current study we examined the effect of normoxic hypercapnia (20% CO2 for 24 h) vs normocapnia (5% CO2), on global gene expression in differentiated normal human airway epithelial cells. Gene expression was assessed on Affymetrix microarrays, and subjected to gene ontology analysis for biological process and cluster-network representation. We found that hypercapnia downregulated the expression of 183 genes and upregulated 126. Among these, major gene clusters linked to immune responses and nucleosome assembly were largely downregulated, while lipid metabolism genes were largely upregulated. The overwhelming majority of these genes were not previously known to be regulated by CO2. These changes in gene expression indicate the potential for hypercapnia to impact bronchial epithelial cell function in ways that may contribute to poor clinical outcomes in patients with severe acute or advanced chronic lung diseases.

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ZFHX3 modulates the androgen/AR signaling activity in prostate cancer cells

Project description:The androgen/androgen receptor (AR) signaling drives prostate development and prostatic carcinogenesis, whereas loss of the zinc finger homeobox 3 (ZFHX3) transcription factor attenuates prostate development and promotes prostatic tumorigenesis. The androgen/AR signaling upregulates the transcription of ZFHX3 in prostate cancer cells. However, whether and how ZFHX3 is involved in the function of AR signaling in prostate cancer cells is unknown. In this study, we first carried out RNA-seq analysis in C4-2B prostate cancer cells to detect what genes and signaling pathways are caused by the deletion of ZFHX3. Gene set enrichment analysis (GSEA) revealed that among the top altered hallmark gene sets after ZFHX3 deletion, only the one for androgen response was decreased, whereas those for TNFα, interferon γ, and inflammatory response were enriched. For the 27 genes indicative AR activities, as defined in a previous study, expression levels for 18 of the 27 genes were significantly changed by ZFHX3 loss. Fifteen of these 18 genes were downregulated, including classical AR target genes KLK3, FKBP5, and TMPRSS2.

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Project description:Zinc-finger homeobox 3 (ZFHX3, also known as ATBF1) suppresses prostatic tumorigenesis. ZFHX3 is frequently found to have numerous deletions in human prostate cancer (PCa). However, the underlying molecular function of ZFHX3 during prostatic tumorigenesis is not well understood. N6-methyladenosine (m6A) modification in RNA plays a critical role in the development of cancers; however, the relationship between ZFHX3 and m6A modification is largely unknown in PCa. In this study, we found that ZFHX3 knockdown decreased total m6A levels through enhancing the transcriptional activity of FTO in PCa cells. Importantly, FTO inhibition suppressed cell proliferation and rescued the promoting function of ZFHX3 knockdown on cell proliferation. In vivo, we verified that FTO was upregulated and ZFHX3 was decreased in PCa patients and that a high level of ZFHX3 is indispensable for low FTO expression and is correlated with better patient survival. Through transcriptome sequencing and Me-RIP sequencing, we revealed that E2F2 and CDKN2C were the direct targets of FTO-mediated m6A modification and ZFXH3 was required for the regulation of FTO on E2F2 and CDKN2C expression. Unexpectedly, we uncovered that ZFHX3 expression was in return regulated by FTO in a m6A-dependent way. These findings establish a novel crosstalk mechanism between ZFHX3 and FTO in prostatic tumorigenesis.

2023-10-31 | GSE244356 | GEO

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