NDLI: Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells

Content Provider	PubMed Central
Author	Checa, Marco Hagood, James S. Rafael, Velazquez-cruz Ruiz, Victor Carolina, García-de-alba Claudia, Rangel-escareño Urrea, Francisco Becerril, Carina Montaño, Martha García-trejo, Semiramis Lira, José Cisneros Arnoldo, Aquino-gálvez Pardo, Annie Selman, Moisés
Editor	Oliver, Eickelberg
Copyright Year	2016
Abstract	Idiopathic pulmonary fibrosis (IPF) is a progressive and lethal disease of unknown etiology. A growing body of evidence indicates that it may result from an aberrant activation of alveolar epithelium, which induces the expansion of the fibroblast population, their differentiation to myofibroblasts and the excessive accumulation of extracellular matrix. The mechanisms that activate the alveolar epithelium are unknown, but several studies indicate that smoking is the main environmental risk factor for the development of IPF. In this study we explored the effect of cigarette smoke on the gene expression profile and signaling pathways in alveolar epithelial cells. Lung epithelial cell line from human (A549), was exposed to cigarette smoke extract (CSE) for 1, 3, and 5 weeks at 1, 5 and 10% and gene expression was evaluated by complete transcriptome microarrays. Signaling networks were analyzed with the Ingenuity Pathway Analysis software. At 5 weeks of exposure, alveolar epithelial cells acquired a fibroblast-like phenotype. At this time, gene expression profile revealed a significant increase of more than 1000 genes and deregulation of canonical signaling pathways such as TGF-β and Wnt. Several profibrotic genes involved in EMT were over-expressed, and incomplete EMT was observed in these cells, and corroborated in mouse (MLE-12) and rat (RLE-6TN) epithelial cells. The secretion of activated TGF-β1 increased in cells exposed to cigarette smoke, which decreased when the integrin alpha v gene was silenced. These findings suggest that the exposure of alveolar epithelial cells to CSE induces the expression and release of a variety of profibrotic genes, and the activation of TGF-β1, which may explain at least partially, the increased risk of developing IPF in smokers.
Related Links	http://dx.doi.org/10.1371/journal.pone.0150383
Starting Page	150383
File Format	PDF
ISSN	19326203
e-ISSN	19326203
Journal	PLoS ONE
Issue Number	3
Volume Number	11
Language	English
Publisher	Public Library of Science
Publisher Date	2016-03-01
Access Restriction	Open
Rights Holder	Public Library of Science
Subject Keyword	Biochemistry, Genetics and Molecular Biology(all) Agricultural and Biological Sciences(all) Medicine(all) Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Human Alveolar Epithelial Cell Injury Induced by Cigarette Smoke

Cigarette Smoke Extract (CSE) Delays NOD2 Expression and Affects NOD2/RIPK2 Interactions in Intestinal Epithelial Cells

Biological Effects of Cigarette Smoke in Cultured Human Retinal Pigment Epithelial Cells

Cigarette Smoke Decreases Airway Epithelial FABP5 Expression and Promotes Pseudomonas aeruginosa Infection

Whole Cigarette Smoke Increased the Expression of TLRs, HBDs, and Proinflammory Cytokines by Human Gingival Epithelial Cells through Different Signaling Pathways

Cigarette Smoke Causes Caspase-Independent Apoptosis of Bronchial Epithelial Cells from Asthmatic Donors

Caspase-12 Silencing Attenuates Inhibitory Effects of Cigarette Smoke Extract on NOD1 Signaling and hBDs Expression in Human Oral Mucosal Epithelial Cells

Cigarette Smoke Decreases the Maturation of Lung Myeloid Dendritic Cells

Functional Interaction between Human Papillomavirus Type 16 E6 and E7 Oncoproteins and Cigarette Smoke Components in Lung Epithelial Cells

Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells

Similar Documents

Human Alveolar Epithelial Cell Injury Induced by Cigarette Smoke

Cigarette Smoke Extract (CSE) Delays NOD2 Expression and Affects NOD2/RIPK2 Interactions in Intestinal Epithelial Cells

Biological Effects of Cigarette Smoke in Cultured Human Retinal Pigment Epithelial Cells

Cigarette Smoke Decreases Airway Epithelial FABP5 Expression and Promotes Pseudomonas aeruginosa Infection

Whole Cigarette Smoke Increased the Expression of TLRs, HBDs, and Proinflammory Cytokines by Human Gingival Epithelial Cells through Different Signaling Pathways

Cigarette Smoke Causes Caspase-Independent Apoptosis of Bronchial Epithelial Cells from Asthmatic Donors

Caspase-12 Silencing Attenuates Inhibitory Effects of Cigarette Smoke Extract on NOD1 Signaling and hBDs Expression in Human Oral Mucosal Epithelial Cells

Cigarette Smoke Decreases the Maturation of Lung Myeloid Dendritic Cells

Functional Interaction between Human Papillomavirus Type 16 E6 and E7 Oncoproteins and Cigarette Smoke Components in Lung Epithelial Cells

Cigarette Smoke Enhances the Expression of Profibrotic Molecules in Alveolar Epithelial Cells