Document Detail


Protein expression profile of rat type two alveolar epithelial cells during hyperoxic stress and recovery.
MedLine Citation:
PMID:  24014686     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In rodent model systems, the sequential changes in lung morphology resulting from hyperoxic injury are well characterized and are similar to changes in human acute respiratory distress syndrome. In the injured lung, alveolar type two (AT2) epithelial cells play a critical role in restoring the normal alveolar structure. Thus characterizing the changes in AT2 cells will provide insights into the mechanisms underpinning the recovery from lung injury. We applied an unbiased systems-level proteomics approach to elucidate molecular mechanisms contributing to lung repair in a rat hyperoxic lung injury model. AT2 cells were isolated from rat lungs at predetermined intervals during hyperoxic injury and recovery. Protein expression profiles were determined by using iTRAQ with tandem mass spectrometry. Of the 959 distinct proteins identified, 183 significantly changed in abundance during the injury-recovery cycle. Gene ontology enrichment analysis identified cell cycle, cell differentiation, cell metabolism, ion homeostasis, programmed cell death, ubiquitination, and cell migration to be significantly enriched by these proteins. Gene set enrichment analysis of data acquired during lung repair revealed differential expression of gene sets that control multicellular organismal development, systems development, organ development, and chemical homeostasis. More detailed analysis identified activity in two regulatory pathways, JNK and miR 374. A novel short time-series expression miner algorithm identified protein clusters with coherent changes during injury and repair. We concluded that coherent changes occur in the AT2 cell proteome in response to hyperoxic stress. These findings offer guidance regarding the specific molecular mechanisms governing repair of the injured lung.
Authors:
Maneesh Bhargava; Sanjoy Dey; Trisha Becker; Michael Steinbach; Baolin Wu; Sang Mee Lee; LeeAnn Higgins; Vipin Kumar; Peter B Bitterman; David H Ingbar; Christine H Wendt
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-09-06
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  305     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2013 Nov 
Date Detail:
Created Date:  2013-11-04     Completed Date:  2014-01-02     Revised Date:  2014-11-04    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L604-14     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Acute Lung Injury / genetics,  metabolism*
Algorithms
Animals
Cells, Cultured
Disease Models, Animal
Hyperoxia / genetics,  metabolism*
Male
Oxidative Stress / physiology*
Oxygen / toxicity
Proteomics*
Pulmonary Alveoli / metabolism*
Rats
Rats, Sprague-Dawley
Respiratory Mucosa / metabolism*
Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
Transcriptome
Grant Support
ID/Acronym/Agency:
1UL1RR033183-01/RR/NCRR NIH HHS; 8UL1TR000114-02/TR/NCATS NIH HHS; KL2 TR000113/TR/NCATS NIH HHS
Chemical
Reg. No./Substance:
S88TT14065/Oxygen
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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