RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia.
Bronchi
/ drug effects
Cell Survival
/ drug effects
Cellular Senescence
/ genetics
Cigarette Smoking
/ adverse effects
Epithelial Cells
/ drug effects
Gene Expression Regulation
/ drug effects
Humans
NF-kappa B
/ genetics
Primary Cell Culture
Reactive Oxygen Species
/ metabolism
Sequence Analysis, RNA
Signal Transduction
/ drug effects
Cigarette smoke
Primary human bronchial epithelial cells
RNA-seq
Replicative senescence
Journal
BMC genomics
ISSN: 1471-2164
Titre abrégé: BMC Genomics
Pays: England
ID NLM: 100965258
Informations de publication
Date de publication:
09 Jan 2019
09 Jan 2019
Historique:
received:
18
05
2018
accepted:
26
12
2018
entrez:
11
1
2019
pubmed:
11
1
2019
medline:
10
4
2019
Statut:
epublish
Résumé
Aging is affected by genetic and environmental factors, and cigarette smoking is strongly associated with accumulation of senescent cells. In this study, we wanted to identify genes that may potentially be beneficial for cell survival in response to cigarette smoke and thereby may contribute to development of cellular senescence. Primary human bronchial epithelial cells from five healthy donors were cultured, treated with or without 1.5% cigarette smoke extract (CSE) for 24 h or were passaged into replicative senescence. Transcriptome changes were monitored using RNA-seq in CSE and non-CSE exposed cells and those passaged into replicative senescence. We found that, among 1534 genes differentially regulated during senescence and 599 after CSE exposure, 243 were altered in both conditions, representing strong enrichment. Pathways and gene sets overrepresented in both conditions belonged to cellular processes that regulate reactive oxygen species, proteasome degradation, and NF-κB signaling. Our results offer insights into gene expression responses during cellular aging and cigarette smoke exposure, and identify potential molecular pathways that are altered by cigarette smoke and may also promote airway epithelial cell senescence.
Sections du résumé
BACKGROUND
BACKGROUND
Aging is affected by genetic and environmental factors, and cigarette smoking is strongly associated with accumulation of senescent cells. In this study, we wanted to identify genes that may potentially be beneficial for cell survival in response to cigarette smoke and thereby may contribute to development of cellular senescence.
RESULTS
RESULTS
Primary human bronchial epithelial cells from five healthy donors were cultured, treated with or without 1.5% cigarette smoke extract (CSE) for 24 h or were passaged into replicative senescence. Transcriptome changes were monitored using RNA-seq in CSE and non-CSE exposed cells and those passaged into replicative senescence. We found that, among 1534 genes differentially regulated during senescence and 599 after CSE exposure, 243 were altered in both conditions, representing strong enrichment. Pathways and gene sets overrepresented in both conditions belonged to cellular processes that regulate reactive oxygen species, proteasome degradation, and NF-κB signaling.
CONCLUSIONS
CONCLUSIONS
Our results offer insights into gene expression responses during cellular aging and cigarette smoke exposure, and identify potential molecular pathways that are altered by cigarette smoke and may also promote airway epithelial cell senescence.
Identifiants
pubmed: 30626320
doi: 10.1186/s12864-018-5409-z
pii: 10.1186/s12864-018-5409-z
pmc: PMC6325884
doi:
Substances chimiques
NF-kappa B
0
Reactive Oxygen Species
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
22Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL135062
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL142997
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL128297
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL125435
Pays : United States
Organisme : NIH HHS
ID : HL114453
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL098174
Pays : United States
Organisme : CSRD VA
ID : I01 CX001048
Pays : United States
Organisme : CSRD VA
ID : I01 CX000105
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL114453
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL096376
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL113105
Pays : United States
Organisme : NHLBI NIH HHS
ID : K23 HL126912
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL123766
Pays : United States
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