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Buffered hypercapnia alters the transcriptional profile in monocytes.

ABSTRACT: Buffered hypercapnia alters the transcriptional profile in monocytes.

PROVIDER: PRJNA850180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19732917_1.fastq.gz	Fastqsanger.gz
	SRR19732917_2.fastq.gz	Fastqsanger.gz
	SRR19732918_1.fastq.gz	Fastqsanger.gz
	SRR19732918_2.fastq.gz	Fastqsanger.gz
	SRR19732919_1.fastq.gz	Fastqsanger.gz

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Buffered hypercapnia alters the transcriptional profile in monocytes.

Project description:In monocytes we used RNA-sequencing to investigate the effect of 4hrs of exposure to buffered hypercapnia (10% CO2) compared to normocapnia (5% CO2) with and without the pro-inflammatory stimulus LPS (2.5ug/ml) for the final 2hrs. Buffered hypercapnia causes transcriptional changes associated with altered metabolic function in both the basal and stimulated states.

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Hypercapnia alters Wnt production from PDGFR+ lung fibroblasts

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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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