| Formaldehyde induces apoptosis through decreased Prx 2 via p38 MAPK in lung epithelial cells. | |
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MedLine Citation:
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PMID: 20347000 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Formaldehyde (FA) is an important substance that induces sick house syndrome and diseases, such as asthma and allergies. Oxidative stress is involved in the development of respiratory disease, and diverse antioxidants may protect respiratory tract cells from apoptosis. Peroxiredoxin is a pivotal endogenous antioxidant. In the present study, FA induced death in A549 cells, a lung epithelial cell line, in a dose-dependent manner. FA also increased lipid peroxide formation (LPO) in A549 cells, suggesting a role for oxidative stress. Additionally, FA decreased peroxiredoxin 2 (Prx 2) protein levels after a 24 or 48h exposure to FA. We also examined whether the FA-induced decrease in Prx 2 was associated with apoptosis. Prx 2 overexpression protected against FA-induced cell apoptosis but not necrosis. Prx 2 overexpression blocked FA-induced increase in Bax, a pro-apoptotic molecule, and a decrease in Bcl-2, an anti-apoptotic molecule. Prx 2 overexpression also protected against FA-induced activation of some special apoptosis-associated proteins [caspase-3, caspase-9, and polypeptide poly (ADP-ribose) polymerase (PARP)]. Furthermore, we examined the signaling molecules involved in the FA-induced decrease in Prx 2 expression. The FA-induced decrease in Prx 2 and increase in cell apoptosis was restored by treatment with SB203580 [a p38 mitogen activated protein kinase (MAPK) inhibitor], but not by SP600125 [a c-jun-N-terminal kinase (JNK) inhibitor]. Also, FA-induced events were blocked by treatment with p38 siRNA, but not by scrambled siRNA. Indeed, FA increased p38 MAPK activation, suggesting a role for p38 MAPK in FA action. In conclusion, FA mediated apoptosis in lung epithelial cells by decreasing Prx 2 via p38 MAPK. |
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Authors:
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Seul Ki Lim; Jong Chun Kim; Chang Jong Moon; Gye Yeop Kim; Ho Jae Han; Soo Hyun Park |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-03-25 |
Journal Detail:
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Title: Toxicology Volume: 271 ISSN: 1879-3185 ISO Abbreviation: Toxicology Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-05-10 Completed Date: 2010-05-20 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0361055 Medline TA: Toxicology Country: Ireland |
Other Details:
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Languages: eng Pagination: 100-6 Citation Subset: IM |
Affiliation:
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Bio-therapy Human Resources Center, College of Veterinary Medicine, Chonnam National University, Yongbongdong 300 Bukgu, Gwangju 500-757, Republic of Korea. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Diphosphate Ribose
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metabolism Apoptosis / physiology* Caspase 3 / metabolism Caspase 9 / metabolism Cell Death Cell Line, Tumor Epithelial Cells / metabolism* Formaldehyde / metabolism* Genes, bcl-2 Humans Lung / metabolism, pathology Oxidative Stress Peroxiredoxins / metabolism* Poly(ADP-ribose) Polymerases / metabolism bcl-2-Associated X Protein / metabolism p38 Mitogen-Activated Protein Kinases / metabolism* |
| Chemical | |
Reg. No./Substance:
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0/bcl-2-Associated X Protein; 20762-30-5/Adenosine Diphosphate Ribose; 50-00-0/Formaldehyde; EC 1.11.1.15/Peroxiredoxins; EC 2.4.2.30/Poly(ADP-ribose) Polymerases; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9 |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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