Involvement of Bcl-2 family in apoptosis and signal pathways induced by cigarette smoke extract in the human airway smooth muscle cells

DNA and Cell Biology
Weihua HuWang Ni

Abstract

Chronic obstructive pulmonary disease (COPD) is a highly prevalent airway disease characterized by an abnormal inflammatory response of the lungs to noxious particles and gases. Cigarette smoking remains a major risk factor for COPD development; however, little is known about its effect on human airway smooth muscle cells (HASMCs). The aim of this study is to examine whether apoptosis is involved in cigarette smoke extract (CSE)-induced HASMC death and the molecular mechanisms underlying it. Our studies have shown that CSE increased the level of reactive oxygen species (ROS) and cell apoptosis of HASMCs in a dose- and time-dependent manner, and the ROS scavenger N-acetyl-cysteine abrogated the effect of ROS level and apoptosis on HASMCs. Further, the expression of Bax, Bad, and Fas was increased but Bcl-2 and nuclear factor-kappaB (NF-kappaB) was decreased in a dose- and time-dependent fashion in CSE-induced apoptosis in HASMCs. Taken together, CSE could inhibit the cell growth and induce apoptosis of HASMCs through both the mitochondrial pathway and death receptor pathway. Oxidative stress and inhibition of NF-kappaB expression caused by CSE may play important roles in apoptosis and inhibition of cell growth in HASMCs.

References

Jan 1, 1992·Free Radical Research Communications·R SchreckP A Baeuerle
Mar 10, 1995·Science·S Nagata, P Golstein
Nov 1, 1996·Science·D J Van AntwerpI M Verma
Apr 10, 1997·The New England Journal of Medicine·P J Barnes, M Karin
Apr 1, 1997·Seminars in Immunology·V Depraetere, P Golstein
Nov 14, 1998·Biochemical and Biophysical Research Communications·M VayssierB S Polla
Aug 4, 1999·Proceedings of the National Academy of Sciences of the United States of America·H H LeeG Cheng
Sep 18, 1999·Free Radical Biology & Medicine·H Wang, J A Joseph
Feb 26, 2000·Annual Review of Genetics·S Nagata
Jun 3, 2000·Annual Review of Immunology·M Karin, Y Ben-Neriah
Feb 16, 2002·Methods : a Companion to Methods in Enzymology·K J Livak, T D Schmittgen
May 2, 2002·Cell·Sankar Ghosh, Michael Karin
Sep 6, 2002·The Journal of Biological Chemistry·Takeyuki NishiHiroshi Handa
Dec 21, 2002·Molecular Immunology·Christoph Borner
Oct 30, 2003·The European Respiratory Journal·P J BarnesR A Pauwels
Nov 25, 2003·Oncogene·Alexei DegterevJunying Yuan
Feb 11, 2004·Chest·Naoko YokohoriUNKNOWN Respiratory Failure Research Group in Japan
Oct 1, 2004·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Fiona M MoodieIrfan Rahman
Dec 4, 2004·FASEB Journal : Official Publication of the Federation of American Societies for Experimental Biology·Anna A BirukovaAlexander D Verin
Feb 3, 2005·The European Respiratory Journal·K ImaiJ M D'Armiento
Feb 26, 2005·The Journal of Biological Chemistry·Xiao-chun BaiShen-qiu Luo
May 24, 2005·Current Opinion in Pharmacology·Ingel K DemedtsRomain A Pauwels
Sep 15, 2005·The Journal of Allergy and Clinical Immunology·Philippe Joubert, Qutayba Hamid
Feb 4, 2006·Monaldi Archives for Chest Disease = Archivio Monaldi Per Le Malattie Del Torace·M Bartal
Feb 7, 2006·Pharmacology & Therapeutics·Paul Kirkham, Irfan Rahman

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Citations

Nov 10, 2010·Cellular and Molecular Neurobiology·Qin LiLianjun Guo
Mar 19, 2013·Respiratory Research·Jun KojimaKazuyoshi Kuwano
Jun 11, 2011·International Journal of Chronic Obstructive Pulmonary Disease·Rahul G Sangani, Andrew J Ghio
Mar 23, 2013·Experimental and Toxicologic Pathology : Official Journal of the Gesellschaft Für Toxikologische Pathologie·Fengjiao YuanWeiyun Zhang
Jul 16, 2014·Archivos de bronconeumología·Jai Prakash MuyalAmit Kumar Tyagi
Nov 26, 2010·International Immunopharmacology·Rossella PaolilloAntonietta Rizzo
Feb 24, 2012·The Korean Journal of Physiology & Pharmacology : Official Journal of the Korean Physiological Society and the Korean Society of Pharmacology·Chul Ho YoonDawon Kang
Dec 8, 2014·International Immunopharmacology·Naixing KangYingqun Zhu
Feb 12, 2019·Environmental Toxicology·Cho-Won KimKyung-Chul Choi
Dec 20, 2018·International Journal of Molecular Sciences·Necola GuerrinaCarolyn J Baglole
Apr 9, 2014·The Journal of Biological Chemistry·Zhihong YuanRuxana T Sadikot
Jan 30, 2010·Current Opinion in Pulmonary Medicine

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