Nicotine inhibits histone deacetylase 6 activity and chaperone-dependent activation of the glucocorticoid receptor in A549 cells.
- Author:
Li-chao SUN
1
;
Jiang-tao LIN
;
Wen LI
;
Lan ZHANG
;
Tong-liang ZHOU
;
Xiao-yan ZHANG
Author Information
- Publication Type:Journal Article
- MeSH: Cell Line, Tumor; Cell Proliferation; drug effects; Enzyme Activation; drug effects; Histone Deacetylase 6; Histone Deacetylases; genetics; metabolism; Humans; Nicotine; pharmacology; Receptors, Glucocorticoid; genetics; metabolism
- From: Chinese Medical Journal 2012;125(4):662-666
- CountryChina
- Language:English
-
Abstract:
BACKGROUNDNicotine, a major component of tobacco, is the main cause of smoking addiction. It was found that asthmatic patients who smoke were insensitive to glucocorticoid treatment. In this paper, we investigated whether nicotine could inhibit histone deacetylase 6 activity (HDAC6) and chaperone-dependent activation of the glucocorticoid receptor (GR) in A549 cells. Furthermore, the expression level of heat shock protein 90 (HSP90) was determined.
METHODSQuantitative real-time polymerase chain reaction was used to detect the levels of RNA transcription, and Western blotting was applied to analyze the levels of protein expression of HDAC6, GR, and HSP90 in A549 cells. Moreover, the effects of dexamethasone and trichostatin A were observed in A549 cells.
RESULTSA549 cell proliferation was inhibited in the presence of nicotine, and the level of RNA and protein expression of HDAC6 and GR were down-regulated.
CONCLUSIONSNicotine could inhibit HDAC6 activity and chaperone-dependent activation of GR. This might be the main reason why asthmatic patients who smoke show insensitivity to the glucocorticoid treatment.
