eCite Digital Repository

Cigarette smoke induces a distinct fibrotic signature in bronchial epithelial cells in comparison to TGFß

Citation

Ge, Q and Krimmer, D and Chen, L and Burgess, J and Black, J and Oliver, BG, Cigarette smoke induces a distinct fibrotic signature in bronchial epithelial cells in comparison to TGFß, American Journal of Respiratory and Critical Care Medicine, May 18-23, 2012, San Francisco, California, pp. 4584. ISSN 0903-1936 (2012) [Conference Extract]


Preview
PDF (2012 Am J Respir Crit Care Med 185;2012:A2021)
Not available
19Kb
  

Abstract

Rationale: We have previously shown cigarette smoke extract (CSE) induces the production of the extracellular matrix proteins fibronectin and perlecan in human lung fibroblasts (Krimmer et al AJRCMB 2011). The proteins were also induced by transforming growth factor β (TGFβ); however the signal transduction pathways activated by CSE were different to those used by TGFβ. These differences lead us to speculate that if we were to look at an increased number of molecules involved in the development of fibrosis, we would find differential upregulation by TGFβ and CSE.

Aim: To compare fibrosis related genes upregulated by TGFβ or CSE in primary human bronchial epithelial (HBE) cells.

Methods: HBE cells were grown to confluence in BEGM in the absence or presence of 5ng/ml of TGFβ1 or 5% CSE. Total RNA were collected after 72 hours. The expression of fibrosis related genes was measured by real time PCR. In total we examined 85 fibrosis related genes. A cut off of a minimum of 1.5 fold induction was used to indicate upregulation of a gene.

Results: TGFβ upregulated 49 different fibrosis associated genes, CSE upregulated only 16, and of all the upregulated genes, 4 were uniquely upregulated by CSE (catenin β1, extracellular matrix protein 1, and TIMP 1 and 2). As expected, TGFβ upregulated a variety of ECM proteins (eg collagen I, IV-VIII, fibronectin); integrins (eg integrin α2, α4-6), and degradative enzymes (eg matrix metalloproteinase (MMP) 1-3, 9-16). In contrast, CSE upregulated only two collagens (XI and XIV) and MMP9.

Conclusion: As CSE selectively upregulated a subset of TGF-β induced genes, elucidation of the specific mechanisms involved is likely to give novel insight into the pathophysiology of COPD.

Item Details

Item Type:Conference Extract
Keywords:Cigarette smoke extract; Bronchial Epithelial Cells; Chronic Obstructive Pulmonary Disease
Research Division:Medical and Health Sciences
Research Group:Cardiorespiratory Medicine and Haematology
Research Field:Respiratory Diseases
Objective Division:Health
Objective Group:Clinical Health (Organs, Diseases and Abnormal Conditions)
Objective Field:Respiratory System and Diseases (incl. Asthma)
Author:Chen, L (Dr Ling Chen)
ID Code:94874
Year Published:2012
Deposited By:Medicine (Discipline)
Deposited On:2014-09-18
Last Modified:2014-10-28
Downloads:0

Repository Staff Only: item control page