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Analysis of cellular senescence induced by lipopolysaccharide in pulmonary alveolar epithelial cells

Authors
 Chang Oh Kim  ;  Ae Jung Huh  ;  Sang Hoon Han  ;  June Myung Kim 
Citation
 ARCHIVES OF GERONTOLOGY AND GERIATRICS, Vol.54(2) : 35-41, 2012 
Journal Title
ARCHIVES OF GERONTOLOGY AND GERIATRICS
ISSN
 0167-4943 
Issue Date
2012
MeSH
Aging/drug effects* ; Aging/physiology ; Antioxidants/pharmacology ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Line ; Dose-Response Relationship, Drug ; Glutathione/pharmacology ; Humans ; Hydrogen Peroxide/metabolism ; Lipopolysaccharides/pharmacology* ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Pulmonary Alveoli/cytology ; Pulmonary Alveoli/drug effects* ; Pulmonary Alveoli/physiology ; Respiratory Mucosa/cytology ; Respiratory Mucosa/drug effects* ; Respiratory Mucosa/physiology ; beta-Galactosidase/metabolism
Keywords
Aging/drug effects* ; Aging/physiology ; Antioxidants/pharmacology ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Line ; Dose-Response Relationship, Drug ; Glutathione/pharmacology ; Humans ; Hydrogen Peroxide/metabolism ; Lipopolysaccharides/pharmacology* ; Oxidative Stress/drug effects ; Oxidative Stress/physiology ; Pulmonary Alveoli/cytology ; Pulmonary Alveoli/drug effects* ; Pulmonary Alveoli/physiology ; Respiratory Mucosa/cytology ; Respiratory Mucosa/drug effects* ; Respiratory Mucosa/physiology ; beta-Galactosidase/metabolism
Abstract
In this work, it was examined the possibility of lipopolysaccharide (LPS) causing cellular senescence in lung alveolar epithelial cells. Then, it was clarified how this cellular senescence phenomenon is associated with oxidative stress effect induced by LPS and whether antioxidants could inhibit reduced cellular viability by oxidant stress effect of LPS. In cell viability using cell counting kit-8, exposure to LPS decreased cellular viability and induced growth arrest in a concentration-dependent manner. The pre-apoptotic concentration of LPS was determined by caspase activation using a Caspase-Glo 3/7 luminescence assay kit. This concentration of LPS caused morphologic characteristics shown in senescent cells and elevated senescence-associated β-galactosidase activity. In addition, lysosomal content associated with senescence was increased by LPS at the pre-apoptotic concentration. However, this concentration of LPS did not shorten the telomere length. Exposure to LPS resulted in the formation of hydrogen peroxide in a concentration-dependent manner. The ability of LPS to reduce cellular viability was inhibited by the presence of glutathione. This study revealed that LPS could induce cellular senescence in lung alveloar epithelial cells, and these phenomena were closely associated with hydrogen peroxide production by LPS. Taken together, it is suggested that LPS-induced cellular senescence may play an important role in limiting the tissue repair response after sepsis.
Full Text
http://www.sciencedirect.com/science/article/pii/S016749431100224X
DOI
21871670
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Internal Medicine (내과학교실) > 1. Journal Papers
Yonsei Authors
Kim, June Myung(김준명)
Kim, Chang Oh(김창오) ORCID logo https://orcid.org/0000-0002-0773-5443
Han, Sang Hoon(한상훈) ORCID logo https://orcid.org/0000-0002-4278-5198
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/89610
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