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Cigarette smoke is an endothelial stressor and leads to cell cycle arrest.

Abstract：

:The molecular mechanisms underlying the atherogenic activity of cigarette smoke have yet to be fully elucidated. In the present study, genome-wide microarray analysis was performed on endothelial cells exposed to an aqueous cigarette smoke extract (CSE) for 3, 7, and 24 h, to obtain a better insight into how smoking may lead to endothelial damage. Microarray analysis showed the transcriptional response to CSE was dominated by heat shock, stress responsive, and inflammatory genes, along with genes encoding for anti-oxidant and metal detoxification proteins. The heat shock response was shown to be a result of short lived reactive species of CSE, with the abrogation of the effect by the addition of old CSE, the anti-oxidant N-acetyl cysteine, or the removal of metals from CSE implying that reactive oxygen species are the main culprit. This was further supported by a strong decline in the level of intracellular protein oxidation levels seen under these conditions compared to freshly prepared CSE. Mitochondrial integrity was also found to be significantly compromised after CSE treatment, resulting in a threefold increase in depolarised mitochondria after 6 h. Finally, cell cycle analysis showed the induction of G1 cell cycle arrest. An increased stress and inflammation response indicates that endothelial damage from smoking could contribute to immune cell infiltration, while decreased growth rates reduce endothelial layer repair, promoting atherogenesis.

journal_name

Atherosclerosis

journal_title

Atherosclerosis

authors

Henderson B,Csordas A,Backovic A,Kind M,Bernhard D,Wick G

doi

10.1016/j.atherosclerosis.2008.02.022

subject

Has Abstract

pub_date

2008-12-01 00:00:00

pages

298-305

issue

2

eissn

0021-9150

issn

1879-1484

pii

S0021-9150(08)00127-5

journal_volume

201

pub_type

杂志文章

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