Dataset Information

Time-series proteomics and phosphoproteomics analysis of human airway epithelial cells in the absence or presence of a specific IKK inhibitor

ABSTRACT: Epithelial-mesenchymal transition (EMT) plays a critical role in airway injury, repair, and structural remodeling. Although NFkB/RelA subnit is involved in late EMT-associated gene expression, RelA translocation is occurs later than early phases of IκB kinase (IKK)-depenedent gene expression. To investigate the hypothesis that IKK plays an independent mechanism in TGF-induced EMT, we conducted time-series proteomics and phosphoproteomics analysis of human airway epithelial cells in the absence or presence of a specific IKK inhibitor, BMS -345541.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Lung, Epithelial Cell

SUBMITTER: Yingxin Zhao

LAB HEAD: Yingxin Zhao, Ph.D.

PROVIDER: PXD023531 | Pride | 2022-10-13

REPOSITORIES: Pride

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Publications

Crosstalk of the IκB Kinase with Spliced X-Box Binding Protein 1 Couples Inflammation with Glucose Metabolic Reprogramming in Epithelial-Mesenchymal Transition.

Zhao Yingxin Y Zhang Jing J Sun Hong H Brasier Allan R AR

Journal of proteome research 20210614 7

Epithelial-mesenchymal transition (EMT) plays a critical role in airway injury, repair, and structural remodeling. IκB kinase (IKK)-NFκB signaling regulates late EMT-associated gene expression. However, IKK-mediated mesenchymal transition occurs earlier than NFκB/RelA subunit-dependent EMT gene expression, leading us to investigate the hypothesis that IKK plays an independent mechanism in transforming growth factor-β (TGFβ)-induced EMT. Time-resolved dissection of early proteome and phosphoprote ...[more]

PMID: 34124911

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Project description:Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers; The microarray data deposited here is from 44 HuGeneFL GeneChips, from 9 normal non-smokers and 13 phenotypic normal smokers, large airways, 2 samples per individual, one from the right lung and one from the left lung. These samples were previously described in Hackett NR, Heguy A, Harvey BG, O'Connor TP, Luettich K, Flieder DB, Kaplan R, Crystal RG. Variability of antioxidant-related gene expression in the airway epithelium of cigarette smokers. Am J Respir Cell Mol Biol. 2003 29:331-43 and in Heguy A, Harvey BG, O'Connor TP, Hackett NR, Crystal RG. Sampling-dependent up-regulation of gene expression in sequential samples of human airway epithelial cells. Mol Med. 2003 9:200-8. These data are part of a study aimed at understanding how cigarette smoking modifies neuroendocrine cells, in which microarray analysis with TaqMan confirmation was used to assess airway epithelial samples obtained by fiberoptic bronchoscopy from 81 individuals (normal nonsmokers, normal smokers, smokers with early COPD and smokers with established COPD). Of 11 genes considered to be neuroendocrine cell-specific, only ubiquitin C-terminal hydrolase L1(UCHL1), a member of the ubiquitin proteasome pathway, was consistently upregulated in smokers compared to nonsmokers. Up-regulation of UCHL1 at the protein level was observed with immunohistochemistry of bronchial biopsies of smokers compared to nonsmokers. Interestingly, however, while UCHL1 expression was present only in neuroendocrine cells of the airway epithelium in nonsmokers, UCHL1 expression was also expressed in ciliated epithelial cells in smokers, an intriguing observation in light of recent observations that ciliated cells can are capable of transdifferentiating to other airway epithelium. In the context that UCHL1 is involved in the degradation of unwanted, misfolded or damaged proteins within the cell and is overexpressed in >50% of lung cancers, its overexpression in chronic smokers may represent an early event in the complex transformation from normal epithelium to overt malignancy. Experiment Overall Design: comparison of gene expression in airway epithelial cells of the large airways of phenotypic normal smokers vs normal non-smokers

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