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Effect of Carbon Dioxide on Neonatal Mouse Lung: A Genomic Approach

ABSTRACT: Rationale: Despite the deleterious effects associated with elevated carbon dioxide (CO2), or hypercapnia, it has been hypothesized that CO2 can protect the lung from injury. However, the effects of chronic hypercapnia on the neonatal lung are unknown. Objectives: To determine whether chronic hypercapnia alters alveolar development and to identify genes that could potentially contribute to hypercapnia-mediated lung protection. Methods: Newborn mouse litters were exposed to 8% CO2, 12% CO2 or room air for 2 weeks. Lungs were excised and analyzed for morphometric alterations. Gene expression changes were assessed by microarray techniques and RT-PCR, and gene products by western blotting. Results: The alveolar walls of CO2-exposed mice appeared thinner than those of controls. In addition, genes from a variety of functional categories were differentially expressed with hypercapnia, including those involved with cell growth/maintenance, signal transduction, protein metabolism, ion transport, stress response and inflammation. In particular and of major interest, gene expression was increased for surfactant proteins (SP) A and D, epithelial Na+ channel, GATA binding protein 6 and fibroblast growth factor receptor 2. In addition, SP-A and SP-D protein expression was increased with hypercapnia. Conclusions: Our results lead us to conclude that: 1) There are potentially a number of gene families which may contribute to hypercapnia-mediated lung protection, and 2) up-regulation of SP-A and SP-D may play a role as anti-inflammatory or antioxidant agents. Based on our genomic results, the effects of CO2 depend on the level to which the lung is exposed. Keywords: stress response

ORGANISM(S): Mus musculus

PROVIDER: GSE3161 | GEO | 2006/02/17

SECONDARY ACCESSION(S): PRJNA92997

REPOSITORIES: GEO

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Effect of Carbon Dioxide on Neonatal Mouse Lung: A Genomic Approach

Project description:Rationale: Despite the deleterious effects associated with elevated carbon dioxide (CO2), or hypercapnia, it has been hypothesized that CO2 can protect the lung from injury. However, the effects of chronic hypercapnia on the neonatal lung are unknown. Objectives: To determine whether chronic hypercapnia alters alveolar development and to identify genes that could potentially contribute to hypercapnia-mediated lung protection. Methods: Newborn mouse litters were exposed to 8% CO2, 12% CO2 or room air for 2 weeks. Lungs were excised and analyzed for morphometric alterations. Gene expression changes were assessed by microarray techniques and RT-PCR, and gene products by western blotting. Results: The alveolar walls of CO2-exposed mice appeared thinner than those of controls. In addition, genes from a variety of functional categories were differentially expressed with hypercapnia, including those involved with cell growth/maintenance, signal transduction, protein metabolism, ion transport, stress response and inflammation. In particular and of major interest, gene expression was increased for surfactant proteins (SP) A and D, epithelial Na+ channel, GATA binding protein 6 and fibroblast growth factor receptor 2. In addition, SP-A and SP-D protein expression was increased with hypercapnia. Conclusions: Our results lead us to conclude that: 1) There are potentially a number of gene families which may contribute to hypercapnia-mediated lung protection, and 2) up-regulation of SP-A and SP-D may play a role as anti-inflammatory or antioxidant agents. Based on our genomic results, the effects of CO2 depend on the level to which the lung is exposed. Total 5 arrays including 2 dye-swaps were performed for the 8% CO2 treated animals. Five individual animals were analyzed. Total 4 arrays including 2 dye-swaps were performed for the 12% CO2 treated animals. Four individual animals were analyzed.

2010-07-01 | E-GEOD-3161 | biostudies-arrayexpress

Effect of Hypercapnia on Murine Ventilator-Induced Lung Injury

Project description:Addition of CO2 to the inspired gas can ameliorate lung injury during high tidal volume mechanical ventilation in animal models. Although some effects of hypercapnia on physiology and cell signaling have been characterized, we hypothesized that assessment of genome-wide gene expression patterns would reveal novel pathways of protection. We subjected male C57BL/6J mice to non-injurious low stretch (tidal vol = 10 mL/kg, PEEP = 2 cm H2O) or injurious high stretch (tidal volume approx 35 mL/kg, PEEP = 0 cm H2O) mechanical ventilation for 3 hours under normocapnia (FiCO2 = 0) or hypercapnia (FiCO2 = 0.12).

2017-02-22 | GSE86229 | GEO

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.

2018-09-11 | GSE110362 | GEO

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

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 | GSE243969 | GEO

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

2024-01-21 | GSE183922 | GEO

Drosophila elevated CO2 (hypercapnia) microarray

Project description:The effects of elevated CO2 (hypercapnia) on organisms are not well known, nor are the molecular pathways by which organisms sense CO2. We have performed microarray analysis on Drosophila in order to develop a genetic model for better understanding the effects of CO2. Equal numbers of 5-day old male and female flies (at least 40 total) were exposed to 13% CO2 or air for 24h and RNA extracted. Gene expression changes in CO2 compared with air were analyzed. Experiments were performed in triplicate and the 3 separate microarray experiments are included.

2010-06-25 | E-GEOD-17444 | biostudies-arrayexpress

Drosophila elevated CO2 (hypercapnia) microarray

2009-09-30 | GSE17444 | GEO

Hypercapnia impairs AT2 cell progenitor activity and promotes differentiation to AT1 cells

Project description:Hypercapnia has deleterious effects on cell function, including inhibition of alveolar epithelial cells (AEC) and fibroblast proliferation without causing cell death. Classical studies and lineage-trace models demonstrated that surfactant-producing AT2 cells can serve as stem cells for the structurally and functionally distinct alveolar type 1 cells (AT1) This AT2 reprogramming depends on Wnt/βcat signaling, a pathway that plays critical roles in tissue development and homeostasis throughout the organism lifespan. We found that high CO2 inhibits AT2 cell proliferation and self renewal, and promote their differentiation to ATEC and AT1 cells

2021-12-31 | GSE139426 | GEO

Gene expression profiles in rat alveolar macrophages exposure to submicron carbon fibers

Project description:To evaluate the biological effects at the transcriptional level of manufactured nanomaterials, whole genome microarrays of rat alveolar macrophages (NR8383) exposed to three types of submicron-diameter carbon fibers (SCFs) with different physicochemical properties were performed. In comparison with the fibers of SCF1, the fibers of SCF2 were shorter, and the fibers of SCF3 were thinner.

2021-09-10 | GSE178083 | GEO

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.

2023-04-07 | GSE206333 | GEO

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