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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Genome-wide analysis of lung antigen presenting cells gene expression from cigarette smoke exposed mice

ABSTRACT: Lung antigen presenting cells isolated from wild type but not Spp1-/- mice induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung antigen presenting cells from cigarette smoke exposed mice. These genes may play crucial roles in directing Th1 and Th17 cells differentiation. Lung antigen presenting cells were isolated from lungs of two groups of wild type and Spp1-/- mice that have been exposed to cigarette smoke for 4 months. Total mRNA was extracted from these samples.

ORGANISM(S): Mus musculus

SUBMITTER: Farrah Kheradmand

PROVIDER: E-GEOD-30906 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis of lung antigen presenting cells gene expression from cigarette smoke exposed mice

Project description:Lung antigen presenting cells isolated from wild type but not Spp1-/- mice induce Th1 and Th17 cells differentiation. The goal of this study is to identify the genes differentially expressed by lung antigen presenting cells from cigarette smoke exposed mice. These genes may play crucial roles in directing Th1 and Th17 cells differentiation.

2011-08-01 | GSE30906 | GEO

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

Project description:Analysis of lung CD11c+ antigen presenting cells (APCs) isolated from wildtype or Mir22-/- mice exposed to nanoparticulate carbon black (nCB) for one month. MiR-22 plays important roles in nCB induced experimental emphysema through regulating APC activation. Results provide insight into the biological role and target genes of miR-22. Smoking-related emphysema is a chronic inflammatory disease driven by T helper 17 (TH17) cells through molecular mechanisms that remain obscure. Here we have explored the role of microRNA-22 (miR-22) in emphysema. MiR-22 was upregulated in lung myeloid dendritic cells (mDCs) of smokers with emphysema and antigen-presenting cells (APCs) of mice exposed to smoke or nanoparticulate carbon black (nCB) through a mechanism involving NF-kappaB. MiR-22-deficient mice, but not wild-type, showed attenuated TH17 responses and failed to develop emphysema after exposure to either smoke or nCB. We further show that miR-22 controls APC activation and TH17 responses through activation of AP-1 transcription factor complexes and histone deacetylase (HDAC) 4. Thus, miR-22 is a critical regulator of both emphysema and TH17 responses. Lung APCs were isolated from PBS (reference groups) or nCB exposed wildtype or Mir22-/- mice, total four groups. There were three replicates in each group.

2015-09-05 | E-GEOD-72734 | biostudies-arrayexpress

Genome-wide analysis of microRNA-22 responsive gene expression in lung antigen presenting cells in response to chronic nanoparticulate carbon black exposure

2015-09-05 | GSE72734 | GEO

Mus musculus

Project description:Genome-wide analysis of lung antigen presenting cells gene expression from cigarette smoke exposed mice

| PRJNA144225 | ENA

Cigarette smoke induces mitochondrial metabolic reprogramming in lung cells

Project description:Cigarette smoking remains the leading cause of non-small cell lung carcinoma. Studies involving acute exposure of smoke on lung cells revealed induction of pre- cancerous state in lung cells. Recently few studies have reported the chronic effect of cigarette smoke in inducing cellular transformation. Yet no systemic study has been performed to understand the molecular alterations in lung cells due to cigarette smoke. Hence it is both important and necessary to study the chronic effect of cigarette smoke in a temporal setting to understand the molecular alterations. In this study, we carried out TMT based proteomic profiling of lung cells which were exposed to cigarette smoke condensate (CSC) for upto 12 months. We identified 2621 proteins in total, of which 145, 114, 87, 169 and 671 proteins were differentially expressed (p<0.05, 1.5 fold) in 2nd, 4th, 6th, 8th and 12th month respectively. Pathway analysis revealed enrichment of xenobiotic metabolism signaling for the first 8 months of smoke treatment, where as continued exposure of smoke for 12 months revealed mitochondrial reprogramming in cells which includes dysregulation of oxidative phosphorylation machinery leading to enhanced reactive oxygen species and higher expression of enzymes involved in tricarboxylic acid cycle (TCA). In addition, chronic exposure of smoke led to overexpression of enzymes involved in glutamine metabolism, fatty acid degradation and lactate synthesis. This could possibly explain the availability of alternative source of carbon in TCA cycle apart from glycolytic pyruvate. Our data indicates that chronic exposure to cigarette smoke induces mitochondrial metabolic transformation in cells to support growth and survival.

2022-03-02 | PXD007108 | Pride

Dissecting the molecular effects of cigarette smoke on proteasome function

Project description:Proteasome dysfunction is emerging as a novel pathomechanism for the development of chronic obstructive pulmonary disease (COPD), a major leading cause of death in the world. Cigarette smoke is one of the main risk factors for COPD and has been shown to impair proteasome function in vitro and in vivo. Importantly, proteasome activity is inhibited in COPD lungs while expression levels of proteasome subunits are not altered. In the present study, we dissected the molecular changes induced by cigarette smoke on proteasome function in lung epithelial cells and mouse lungs. We analyzed the integrity, composition, and the interactome of isolated 26S proteasome complexes from smoke-exposed cells and mouse lungs. Moreover, we applied native MS analysis to investigate whether reactive compounds of cigarette smoke directly modify and inhibit the 20S proteasome complex. Our data reveal that the 20S proteasome is slightly destabilized in the absence of any dominant modification of proteasomal proteins. 26S pulldown and stoichiometry analysis indicated that 26S proteasome complexes become instable in response to cigarette smoke exposure. Of note, the interactome of the 26S was clearly altered in smoke-exposed mouse lungs possibly reflecting an altered cellular composition in the lungs of the smoke-exposed mice. Taken together, our results suggest that cigarette smoke induces minor but detectable changes in the stability and interactome of 20S and 26S proteasome complexes which might contribute in a chronic setting to imbalanced proteostasis as observed in chronic lung diseases associated with cigarette smoking.

2019-01-08 | PXD007148 | Pride

Investigating the impact of cigarette smoke on pulmonary cellular immune responses to influenza virus at the single cell resolution in mice.

Project description:Single cell RNA-sequencing (scRNAseq) of lung immune cells from mice exposed to room air or cigarette smoke, infected with influenza A virus. Room air saline controls are also included. This analysis facilitates a comparison of cigarette smoke-associated changes to the pulmonary immune environment at the level of individual leukocytes and stromal cells.

2022-01-03 | GSE186976 | GEO

Effect of cigarette smoke on microRNA expression in H292 lung cancer cells

Project description:Cigarette smoke has been associated with the development of various lung diseases including cancer. Dysregulation of miRNAs is known to affect protein expression which leads to diverse functional consequences. Investigating miRNA and protein expression in response to cigarette smoke exposure can lead to the identification of potential therapeutic and chemopreventive targets. We employed a SILAC-based quantitative proteomic analysis to identify proteins differentially expressed in response to cigarette smoke in H292 lung cancer cells. LC-MS/MS analysis led to the identification of 3,959 proteins, of which, 303 proteins were overexpressed and 112 proteins were found to be downregulated in cigarette smoke-treated H292 cells.

2018-10-25 | PXD003086 | Pride

mouse lung resistance or sensitivity to cigarette smoke

2008-07-10 | GSE12036 | GEO

Transcription profiling of mouse lung resistance or sensitivity to cigarette smoke

Project description:We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. Experiment Overall Design: Three strains of mice were exposed to smoke from three cigarette/day, 5d/wk for 4 weeks. Microarray analysis was carried out on total RNA extracted from the lung utilizing the Affymetrix platform.

2008-10-21 | E-GEOD-12036 | biostudies-arrayexpress

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