10.1021/pr400998n.s002
Isaac
K. Sundar
Isaac
K.
Sundar
Michael Z. Nevid
Michael Z.
Nevid
Alan E. Friedman
Alan E.
Friedman
Irfan Rahman
Irfan
Rahman
Cigarette Smoke Induces Distinct
Histone Modifications
in Lung Cells: Implications for the Pathogenesis of COPD and Lung Cancer
American Chemical Society
2014
Lung CancerCigarette smoke
posttranslational histone modification patterns
H 292 cells
PTM
histones H 3
H 4
lung diseases
novel histone marks
drive gene expression
CS exposure
Cigarette Smoke Induces Distinct Histone Modifications
COPD
histone H 3
lung cells
histone H 4
2014-02-07 00:00:00
Dataset
https://acs.figshare.com/articles/dataset/Cigarette_Smoke_Induces_Distinct_Histone_Modifications_in_Lung_Cells_Implications_for_the_Pathogenesis_of_COPD_and_Lung_Cancer/2325910
Cigarette smoke (CS)-mediated oxidative
stress induces several
signaling cascades, including kinases, which results in chromatin
modifications (histone acetylation/deacetylation and histone methylation/demethylation).
We have previously reported that CS induces chromatin remodeling in
pro-inflammatory gene promoters; however, the underlying site-specific
histone marks formed in histones H3 and H4 during CS exposure in lungs <i>in vivo</i> and in lung cells <i>in vitro</i>, which
can either drive gene expression or repression, are not known. We
hypothesize that CS exposure in mouse and human bronchial epithelial
cells (H292) can cause site-specific posttranslational histone modifications
(PTMs) that may play an important role in the pathogenesis of CS-induced
chronic lung diseases. We used a bottom-up mass spectrometry approach
to identify some potentially novel histone marks, including acetylation,
monomethylation, and dimethylation, in specific lysine and arginine
residues of histones H3 and H4 in mouse lungs and H292 cells. We found
that CS-induced distinct posttranslational histone modification patterns
in histone H3 and histone H4 in lung cells, which may be considered
as usable biomarkers for CS-induced chronic lung diseases. These identified
histone marks (histone H3 and histone H4) may play an important role
in the epigenetic state during the pathogenesis of smoking-induced
chronic lung diseases, such as chronic obstructive pulmonary disease
and lung cancer.