Imperial College London
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RESEARCH TECHNICIAN

Faculty of Medicine, National Heart & Lung Institute

Research Technician
 
 
 
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Contact

 

+44 (0)20 7594 7897p.fenwick

 
 
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Location

 

Technician Room 229BGuy Scadding BuildingRoyal Brompton Campus

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Summary

 

Publications

Citation

BibTex format

@article{Yanagisawa:2018:10.1371/journal.pone.0193921,
author = {Yanagisawa, S and Baker, JR and Vuppusetty, C and Koga, T and Colley, T and Fenwick, P and Donnelly, LE and Barnes, PJ and Ito, K},
doi = {10.1371/journal.pone.0193921},
journal = {PLoS ONE},
title = {The dynamic shuttling of SIRT1 between cytoplasm and nuclei in bronchial epithelial cells by single and repeated cigarette smoke exposure},
url = {http://dx.doi.org/10.1371/journal.pone.0193921},
volume = {13},
year = {2018}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - SIRT1 (silent information regulator 2 homolog 1) is a crucial cellular survival protein especially in oxidative stress environments, and has been thought to locate within the nuclei, but also known to shuttle between cytoplasm and nuclei in some cell types. Here, we show for the first time the dynamics of SIRT1 in the presence of single or concurrent cigarette smoke extract (CSE) exposure in human bronchial epithelial cells (HBEC). In BEAS-2B HBEC or primary HBEC, SIRT1 was localized predominantly in cytoplasm, and the CSE (3%) induced nuclear translocation of SIRT1 from cytoplasm in the presence of L-buthionine sulfoximine (an irreversible inhibitor of γ-glutamylcystein synthetase), mainly through the activation of phosphatidylinositol 3-kinase (PI3K) α subunit. This SIRT1 nuclear shuttling was associated with FOXO3a nuclear translocation and the strong induction of several anti-oxidant genes including superoxide dismutase (SOD) 2 and 3; therefore seemed to be an adaptive response. When BEAS-2B cells were pretreated with repeated exposure to a lower concentration of CSE (0.3%), the CSE-induced SIRT1 shuttling and resultant SOD2/3 mRNA induction were significantly impaired. Thus, this result offers a useful cell model to mimic the impaired anti-oxidant capacity in cigarette smoking-associated lung disease such as chronic obstructive pulmonary disease.
AU  - Yanagisawa,S
AU  - Baker,JR
AU  - Vuppusetty,C
AU  - Koga,T
AU  - Colley,T
AU  - Fenwick,P
AU  - Donnelly,LE
AU  - Barnes,PJ
AU  - Ito,K
DO  - 10.1371/journal.pone.0193921
PY  - 2018///
SN  - 1932-6203
TI  - The dynamic shuttling of SIRT1 between cytoplasm and nuclei in bronchial epithelial cells by single and repeated cigarette smoke exposure
T2  - PLoS ONE
UR  - http://dx.doi.org/10.1371/journal.pone.0193921
UR  - https://www.ncbi.nlm.nih.gov/pubmed/29509781
UR  - http://hdl.handle.net/10044/1/58025
VL  - 13
ER  -
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