Effects of cigarette smoke extract on A549 cells and human lung fibroblasts treated with transforming growth factor-β1 in a coculture system

Liu, Yin; Gao, Wei; Zhang, Deping

doi:10.1007/s10238-009-0081-x

Cited by 48 publications

(37 citation statements)

References 30 publications

(36 reference statements)

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“…In the present work, we have used 2.5% CSE, which is in agreement with the low doses of CSE demonstrating proliferative effects in previous studies [24][25][26], which support fibroblast activation in the process of myofibroblast transition [28].…”

Section: Discussionsupporting

confidence: 66%

“…To that end, one can perform a dose-response and time-course analysis and make some crude calculations to suggest that exposure mimics what might happen in vivo. Thus, for example, low concentrations of CSE (,5%) have shown proliferative effects on lung fibroblasts [24][25][26], while higher (.10%) concentrations showed inhibitory effects on lung fibroblast proliferation [27], thus indicating that among the ,6,000 substance of cigarette smoke, there are some proliferative and other anti-proliferative compounds that may act depending on their final balance.…”

Section: Discussionmentioning

confidence: 99%

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Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition

Milara

Serrano

Peiró³

et al. 2012

Eur Respir J

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Cigarette smoking contributes to lung remodelling in chronic obstructive pulmonary disease (COPD). As part of this remodelling, peribronchiolar fibrosis is observed in the small airways of COPD patients and contributes to airway obstruction. Fibroblast-to-myofibroblast transition is a key step in peribronchiolar fibrosis formation.This in vitro study examined the effect of cigarette smoke on bronchial fibroblast-tomyofibroblast transition, and whether aclidinium bromide inhibits this process. Human bronchial fibroblasts were incubated with aclidinium bromide (10 -9 -10 -7 M) and exposed to cigarette smoke extract. Collagen type I and a-smooth muscle actin (a-SMA) expression were measured by realtime PCR and Western blotting, as myofibroblast markers. Intracellular reactive oxygen species, cyclic AMP (cAMP), extracellular signal-regulated kinase (ERK)1/2 and choline acetyltransferase were measured as intracellular signalling mediators. Cigarette smoke-induced collagen type I and a-SMA was mediated by the production of reactive oxygen species, the depletion of intracellular cAMP and the increase of ERK1/2 phosphorylation and choline acetyltransferase. These effects could be reversed by treatment with the anticholinergic aclidinium bromide, by silencing the mRNA of muscarinic receptors M1, M2 or M3, or by the depletion of extracellular acetylcholine by treatment with acetylcholinesterase.A non-neuronal cholinergic system is implicated in cigarette smoke-induced bronchial fibroblast-to-myofibroblast transition, which is inhibited by aclidinium bromide.

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Section: Discussionsupporting

confidence: 66%

Section: Discussionmentioning

confidence: 99%

Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition

Milara

Serrano

Peiró³

et al. 2012

Eur Respir J

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“…Besides toxicity induced cell destruction, CSE might also inhibit cell proliferation (Jiao et al 2006). Liu et al demonstrated that cigarette smoke decreased the proliferation of alveolar cells, partly by induction of pro-inflammatory cytokines resulting in inflammation that contributed to alveolar cell damage (Liu et al 2009). …”

Section: Discussionmentioning

confidence: 99%

“…It contains 10 14 -10 16 free radicals/puff, disturbing the oxidantantioxidant balance leading to cellular damage in the lungs. It has been shown that in response to cigarette smoke, apoptosis and necrosis of the alveolar wall cells occurs (Liu et al 2009). This destruction results in progressive cell loss and airway enlargement: the prominent features of emphysema (Demedts et al 2006).…”

Section: Introductionmentioning

confidence: 99%

Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells

Gál

Aron

Szalay

et al. 2011

Cell Stress and Chaperones

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Smoking is the leading risk factor of chronic obstructive pulmonary disease (COPD) and lung cancer. Corticosteroids are abundantly used in these patients; however, the interaction of smoking and steroid treatment is not fully understood. Heat shock proteins (Hsps) play a central role in the maintenance of cell integrity, apoptosis and cellular steroid action. To better understand cigarette smoke-steroid interaction, we examined the effect of cigarette smoke extract (CSE) and/or dexamethasone (DEX) on changes of intracellular heat shock protein-72 (Hsp72) in lung cells. Alveolar epithelial cells (A549) were exposed to increasing doses (0; 0.1; 1; and 10 μM/μl) of DEX in the medium in the absence(C) and presence of CSE. Apoptosis, necrosis, Hsp72 messenger-ribonucleic acid (mRNA) and protein expression of cells were measured, and the role of Hsp72 on steroid effect examined. CSE reduced the number of viable cells by significantly increasing the number of apoptotic and necrotic cells. DEX dose-dependently decreased the ratio of apoptosis when CSE was administered, without change in necrosis. CSE - DEX co-treatment dose-dependently increased Hsp72 mRNA and protein expression, with the highest level measured in CSE + DEX (10) cells, while significantly lower levels were noted in all respective C groups. Pretreatment with Hsp72 silencing RNA confirmed that increased survival observed following DEX administration in CSE-treated cells was mainly mediated via the Hsp72 system. CSE significantly decreases cell survival by inducing apoptosis and necrosis. DEX significantly increases Hsp72 mRNA and protein expression only in the presence of CSE resulting in increased cellular protection and survival. DEX exerts its cell protective effects by decreasing apoptotic cell death via the Hsp72 system in CSE-treated alveolar epithelial cells.

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“…But there are not a great number of studies which have been conducted to examine whether the smoking is associated with the occurrence of pulmonary fibrosis, particularly, in relation to the EMT. It has been reported that the cigarette smoking extract (CSE) triggers the occurrence of EMT at a lower concentration in A549 cell lines and it is also associated with the proliferation of myofibroblasts 14 . These findings suggests that it can be involved in the occurrence of idiopathic pulmonary fibrosis (IPF).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of Plasminogen Activator Inhibitor-1 Expression in Smoke-Exposed Alveolar Type II Epithelial Cells Attenuates Epithelial-Mesenchymal Transition

Song

Kang

2011

Tuberc Respir Dis

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Background: Smoking is a risk factor for idiopathic pulmonary fibrosis (IPF), but the mechanism of the association remains obscure. There is evidence demonstrating that plasminogen activator inhibitor-1 (PAI-1) is involved in the progression of pulmonary fibrosis. This study was to determine whether the administration of small interfering RNA (siRNA) targeting PAI-1 or PAI-1 inhibitor to the cigarette smoking extract (CSE)-exposed rat alveolar type II epithelial cells (ATII cells) limits the epithelial-mesenchymal transition (EMT). Methods: ATII cells were isolated from lung of SD-rat using percoll gradient method and cultured with 5% CSE. The EMT was determined from the ATII cells by measuring the real-time RT PCR and western blotting after the PAI-1 siRNA transfection to the cells and after administration of tiplaxtinin, an inhibitor of PAI-1. The effect of PAI-1 inhibitor was also evaluated in the bleomycin-induced rats. Results: PAI-1 was overexpressed in the smoking exposed ATII cells and was directly associated with EMT. The EMT from the ATII cells was suppressed by PAI-1 siRNA transfection or administration of tiplaxtinin. Signaling pathways for EMT by smoking extract were through the phosphorylation of SMAD2 and ERK1/2, and finally Snail expression. Tiplaxtinin also suppressed the pulmonary fibrosis and PAI-1 expression in the bleomycin-induced rats. Conclusion: Our data shows that CSE induces rat ATII cells to undergo EMT by PAI-1 via SMAD2-ERK1/2-Snail activation. This suppression of EMT by PAI-1 siRNA transfection or PAI-1 inhibitor in primary type II alveolar epithelial cells might be involved in the attenuation of bleomycin-induced pulmonary fibrosis in rats.

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Effects of cigarette smoke extract on A549 cells and human lung fibroblasts treated with transforming growth factor-β1 in a coculture system

Cited by 48 publications

References 30 publications

Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition

Aclidinium inhibits cigarette smoke-induced lung fibroblast-to-myofibroblast transition

Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells

Inhibition of Plasminogen Activator Inhibitor-1 Expression in Smoke-Exposed Alveolar Type II Epithelial Cells Attenuates Epithelial-Mesenchymal Transition

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