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

Krisztina Gál, Áron Cseh, Balázs Szalay, K. Rusai, A. Vannay, József Lukácsovits, Uwe Heemann, Attila J. Szabó, G. Losonczy, L. Tamási, V. Müller

Research output: Contribution to journalArticle

17 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)369-378
Number of pages10
JournalCell Stress and Chaperones
Volume16
Issue number4
DOIs
Publication statusPublished - Jul 2011

Fingerprint

HSP72 Heat-Shock Proteins
Alveolar Epithelial Cells
Smoke
Tobacco Products
Dexamethasone
Steroids
RNA
Apoptosis
Necrosis
Cells
Lung Neoplasms
Epithelial Cells
Smoking
Pulmonary diseases
Proteins
Cell death
Heat-Shock Proteins
RNA Interference
Cell Extracts
Chronic Obstructive Pulmonary Disease

Keywords

  • Cigarette smoke
  • COPD
  • Dexamethasone
  • Emphysema
  • Hsp72
  • Lung cancer

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology

Cite this

Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells. / Gál, Krisztina; Cseh, Áron; Szalay, Balázs; Rusai, K.; Vannay, A.; Lukácsovits, József; Heemann, Uwe; Szabó, Attila J.; Losonczy, G.; Tamási, L.; Müller, V.

In: Cell Stress and Chaperones, Vol. 16, No. 4, 07.2011, p. 369-378.

Research output: Contribution to journalArticle

Gál, Krisztina ; Cseh, Áron ; Szalay, Balázs ; Rusai, K. ; Vannay, A. ; Lukácsovits, József ; Heemann, Uwe ; Szabó, Attila J. ; Losonczy, G. ; Tamási, L. ; Müller, V. / Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells. In: Cell Stress and Chaperones. 2011 ; Vol. 16, No. 4. pp. 369-378.
@article{a7649bcca48a440db487e8b3f3568364,
title = "Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells",
abstract = "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.",
keywords = "Cigarette smoke, COPD, Dexamethasone, Emphysema, Hsp72, Lung cancer",
author = "Krisztina G{\'a}l and {\'A}ron Cseh and Bal{\'a}zs Szalay and K. Rusai and A. Vannay and J{\'o}zsef Luk{\'a}csovits and Uwe Heemann and Szab{\'o}, {Attila J.} and G. Losonczy and L. Tam{\'a}si and V. M{\"u}ller",
year = "2011",
month = "7",
doi = "10.1007/s12192-010-0249-z",
language = "English",
volume = "16",
pages = "369--378",
journal = "Cell Stress and Chaperones",
issn = "1355-8145",
publisher = "Springer Netherlands",
number = "4",

}

TY - JOUR

T1 - Effect of cigarette smoke and dexamethasone on Hsp72 system of alveolar epithelial cells

AU - Gál, Krisztina

AU - Cseh, Áron

AU - Szalay, Balázs

AU - Rusai, K.

AU - Vannay, A.

AU - Lukácsovits, József

AU - Heemann, Uwe

AU - Szabó, Attila J.

AU - Losonczy, G.

AU - Tamási, L.

AU - Müller, V.

PY - 2011/7

Y1 - 2011/7

N2 - 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.

AB - 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.

KW - Cigarette smoke

KW - COPD

KW - Dexamethasone

KW - Emphysema

KW - Hsp72

KW - Lung cancer

UR - http://www.scopus.com/inward/record.url?scp=80052446445&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80052446445&partnerID=8YFLogxK

U2 - 10.1007/s12192-010-0249-z

DO - 10.1007/s12192-010-0249-z

M3 - Article

C2 - 21188663

AN - SCOPUS:80052446445

VL - 16

SP - 369

EP - 378

JO - Cell Stress and Chaperones

JF - Cell Stress and Chaperones

SN - 1355-8145

IS - 4

ER -