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BMC Genomics. 2019 Jan 9;20(1):22. doi: 10.1186/s12864-018-5409-z.

RNA sequencing identifies common pathways between cigarette smoke exposure and replicative senescence in human airway epithelia.

Author information

1
Division of Natural Sciences, New College of Florida, Sarasota, FL, USA.
2
Department of Medicine, University of Pittsburgh, NW628 UPMC Montefiore, 3459 Fifth Avenue, Pittsburgh, PA, 15213, USA.
3
VA Pittsburgh Healthcare System, Pittsburgh, PA, USA.
4
Cardiovascular Institute, Department of Medicine, Allegheny Health Network, Pittsburgh, PA, USA.
5
Vascular Medicine Institute, Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
6
Department of Cell and Molecular Physiology, University of North Carolina, Chapel Hill, NC, USA.
7
Lovelace Respiratory Research Institute, COPD program, Albuquerque, NM, USA.
8
Department of Medicine, University of Pittsburgh, NW628 UPMC Montefiore, 3459 Fifth Avenue, Pittsburgh, PA, 15213, USA. nyunoyat@upmc.edu.
9
VA Pittsburgh Healthcare System, Pittsburgh, PA, USA. nyunoyat@upmc.edu.

Abstract

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:

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:

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.

KEYWORDS:

Cigarette smoke; Primary human bronchial epithelial cells; RNA-seq; Replicative senescence

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