| Hepatic growth factor (HGF) inhibits cigarette smoke extract induced apoptosis in human bronchial epithelial cells. | |
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MedLine Citation:
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PMID: 20850432 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Low concentrations of cigarette smoke induced DNA damage and repair without leading to apoptosis in human bronchial epithelial cells. Higher concentrations of cigarette smoke, however, could induce either apoptosis or necrosis. The current study demonstrated that 15% cigarette smoke extract (CSE) induced apoptosis as evidenced by DNA content profiling (17.8±2.1% vs 10.2±1.6% of control, p<0.05), LIVE/DEAD staining (60.2±2.1% viable cells in CSE-treated vs 86.5±2.3% in control cells, p<0.05), and COMET assay (24.3±0.6% of Apoptotic Index in the cells treated with CSE vs 4.7±0.6% of control, P<0.05). Hepatocyte growth factor (HGF) significantly blocked the cigarette smoke-induced apoptosis as shown by DNA profiling (10.8±1.5% of CSE+HGF, p<0.05), LIVE/DEAD staining (78.5±1.2% in CSE+HGF treated cells, p<0.05), and COMET assay (Apoptotic Index: 10.0±0.8% in CSE+HGF treated cells, P<0.05). This protective effect of HGF on CSE-induced apoptosis was abolished by PI3K inhibitors, wortmannin and LY294002, and by introduction of the dominant negative AKT into the cells. Furthermore, CSE plus HGF could induce phosphorylation of AKT Thr 308 and the pro-apoptotic protein, BAD. These results suggest that HGF modulates cell survival in response to cigarette smoke exposure through the PI3K/AKT signaling pathway. |
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Authors:
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Shinsaku Togo; Hisa Sugiura; Amy Nelson; Tetsu Kobayashi; Xingqi Wang; Koh Kamio; Shin Kawasaki; Peter Bitterman; Stephen I Rennard; Xiangde Liu |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-09-17 |
Journal Detail:
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Title: Experimental cell research Volume: 316 ISSN: 1090-2422 ISO Abbreviation: Exp. Cell Res. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-09 Completed Date: 2011-01-26 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0373226 Medline TA: Exp Cell Res Country: United States |
Other Details:
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Languages: eng Pagination: 3501-11 Citation Subset: IM |
Copyright Information:
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Copyright © 2010 Elsevier Inc. All rights reserved. |
Affiliation:
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Pulmonary, Critical Care, Sleep and Allergy Division, Department of Internal Medicine, University of Nebraska Medical Center, Omaha, NE 68198-5910, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Apoptosis
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drug effects* Apoptosis Regulatory Proteins / metabolism Bronchi / cytology* Caspases / metabolism Cell Survival / drug effects Cells, Cultured DNA / drug effects Enzyme Inhibitors / pharmacology Epithelial Cells / cytology*, drug effects*, metabolism Hepatocyte Growth Factor / pharmacology* Humans Necrosis / chemically induced Phosphatidylinositol 3-Kinases / antagonists & inhibitors, metabolism Phosphorylation / drug effects Proto-Oncogene Proteins c-akt / antagonists & inhibitors, genetics, metabolism Signal Transduction / drug effects Smoke / adverse effects* Tobacco / chemistry* X-Linked Inhibitor of Apoptosis Protein / metabolism bcl-Associated Death Protein / metabolism bcl-X Protein / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Apoptosis Regulatory Proteins; 0/BAD protein, human; 0/BCL2L1 protein, human; 0/Enzyme Inhibitors; 0/HGF protein, human; 0/Smoke; 0/X-Linked Inhibitor of Apoptosis Protein; 0/XIAP protein, human; 0/bcl-Associated Death Protein; 0/bcl-X Protein; 67256-21-7/Hepatocyte Growth Factor; 9007-49-2/DNA; EC 2.7.1.-/Phosphatidylinositol 3-Kinases; EC 2.7.11.1/Proto-Oncogene Proteins c-akt; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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