A key role for NOX4 in epithelial cell death during development of lung fibrosis

The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that...

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Vydané v:	Antioxidants & redox signaling Ročník 15; číslo 3; s. 607
Hlavní autori:	Carnesecchi, Stephanie, Deffert, Christine, Donati, Yves, Basset, Olivier, Hinz, Boris, Preynat-Seauve, Olivier, Guichard, Cecile, Arbiser, Jack L, Banfi, Botond, Pache, Jean-Claude, Barazzone-Argiroffo, Constance, Krause, Karl-Heinz
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	United States 01.08.2011
Predmet:	Animals Apoptosis - drug effects Apoptosis - genetics Bleomycin - pharmacology Cells, Cultured Gene Expression Idiopathic Pulmonary Fibrosis - genetics Idiopathic Pulmonary Fibrosis - metabolism Idiopathic Pulmonary Fibrosis - pathology Male Mice NADPH Oxidase 4 NADPH Oxidases - antagonists & inhibitors NADPH Oxidases - genetics NADPH Oxidases - metabolism Oxidative Stress - genetics Pulmonary Alveoli - drug effects Pulmonary Alveoli - metabolism Pulmonary Alveoli - pathology Reactive Oxygen Species - metabolism Respiratory Mucosa - metabolism Respiratory Mucosa - pathology RNA, Small Interfering - genetics Smad2 Protein - metabolism Transforming Growth Factor beta1 - metabolism
ISSN:	1557-7716, 1557-7716
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Abstract	The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that in lungs of patients with idiopathic lung fibrosis, there is strong expression of NOX4 in hyperplastic alveolar type II cells. To study a possible causative role of NOX4 in the death of alveolar cells, we have generated NOX4-deficient mice. Three weeks after administration of bleomycin, wild-type (WT) mice developed massive fibrosis, whereas NOX4-deficient mice displayed almost normal lung histology, and only little Smad2 phosphorylation and accumulation of myofibroblasts. However, the protective effects of NOX4 deficiency preceded the fibrotic stage. Indeed, at day 7 after bleomycin, lungs of WT mice showed massive increase in epithelial cell apoptosis and inflammation. In NOX4-deficient mice, no increase in apoptosis was observed, whereas inflammation was comparable to WT. In vitro, NOX4-deficient primary alveolar epithelial cells exposed to transforming growth factor-β(1) did not generate ROS and were protected from apoptosis. Acute treatment with the NOX inhibitors also blunted transforming growth factor-β(1)-induced apoptosis. ROS generation by NOX4 is a key player in epithelial cell death leading to pulmonary fibrosis.
AbstractList	The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that in lungs of patients with idiopathic lung fibrosis, there is strong expression of NOX4 in hyperplastic alveolar type II cells.UNLABELLEDThe pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that in lungs of patients with idiopathic lung fibrosis, there is strong expression of NOX4 in hyperplastic alveolar type II cells.To study a possible causative role of NOX4 in the death of alveolar cells, we have generated NOX4-deficient mice.AIMTo study a possible causative role of NOX4 in the death of alveolar cells, we have generated NOX4-deficient mice.Three weeks after administration of bleomycin, wild-type (WT) mice developed massive fibrosis, whereas NOX4-deficient mice displayed almost normal lung histology, and only little Smad2 phosphorylation and accumulation of myofibroblasts. However, the protective effects of NOX4 deficiency preceded the fibrotic stage. Indeed, at day 7 after bleomycin, lungs of WT mice showed massive increase in epithelial cell apoptosis and inflammation. In NOX4-deficient mice, no increase in apoptosis was observed, whereas inflammation was comparable to WT. In vitro, NOX4-deficient primary alveolar epithelial cells exposed to transforming growth factor-β(1) did not generate ROS and were protected from apoptosis. Acute treatment with the NOX inhibitors also blunted transforming growth factor-β(1)-induced apoptosis.RESULTSThree weeks after administration of bleomycin, wild-type (WT) mice developed massive fibrosis, whereas NOX4-deficient mice displayed almost normal lung histology, and only little Smad2 phosphorylation and accumulation of myofibroblasts. However, the protective effects of NOX4 deficiency preceded the fibrotic stage. Indeed, at day 7 after bleomycin, lungs of WT mice showed massive increase in epithelial cell apoptosis and inflammation. In NOX4-deficient mice, no increase in apoptosis was observed, whereas inflammation was comparable to WT. In vitro, NOX4-deficient primary alveolar epithelial cells exposed to transforming growth factor-β(1) did not generate ROS and were protected from apoptosis. Acute treatment with the NOX inhibitors also blunted transforming growth factor-β(1)-induced apoptosis.ROS generation by NOX4 is a key player in epithelial cell death leading to pulmonary fibrosis.CONCLUSIONROS generation by NOX4 is a key player in epithelial cell death leading to pulmonary fibrosis. The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4. Epithelial cell death is a crucial early step in the development of the disease, followed only later by the fibrotic stage. We demonstrate that in lungs of patients with idiopathic lung fibrosis, there is strong expression of NOX4 in hyperplastic alveolar type II cells. To study a possible causative role of NOX4 in the death of alveolar cells, we have generated NOX4-deficient mice. Three weeks after administration of bleomycin, wild-type (WT) mice developed massive fibrosis, whereas NOX4-deficient mice displayed almost normal lung histology, and only little Smad2 phosphorylation and accumulation of myofibroblasts. However, the protective effects of NOX4 deficiency preceded the fibrotic stage. Indeed, at day 7 after bleomycin, lungs of WT mice showed massive increase in epithelial cell apoptosis and inflammation. In NOX4-deficient mice, no increase in apoptosis was observed, whereas inflammation was comparable to WT. In vitro, NOX4-deficient primary alveolar epithelial cells exposed to transforming growth factor-β(1) did not generate ROS and were protected from apoptosis. Acute treatment with the NOX inhibitors also blunted transforming growth factor-β(1)-induced apoptosis. ROS generation by NOX4 is a key player in epithelial cell death leading to pulmonary fibrosis.
Author	Hinz, Boris Arbiser, Jack L Krause, Karl-Heinz Guichard, Cecile Banfi, Botond Preynat-Seauve, Olivier Pache, Jean-Claude Donati, Yves Barazzone-Argiroffo, Constance Carnesecchi, Stephanie Deffert, Christine Basset, Olivier
Author_xml	– sequence: 1 givenname: Stephanie surname: Carnesecchi fullname: Carnesecchi, Stephanie email: stephanie.carnesecchi@unige.ch organization: Department of Pediatrics, Medical School, University of Geneva, Geneva, Switzerland. stephanie.carnesecchi@unige.ch – sequence: 2 givenname: Christine surname: Deffert fullname: Deffert, Christine – sequence: 3 givenname: Yves surname: Donati fullname: Donati, Yves – sequence: 4 givenname: Olivier surname: Basset fullname: Basset, Olivier – sequence: 5 givenname: Boris surname: Hinz fullname: Hinz, Boris – sequence: 6 givenname: Olivier surname: Preynat-Seauve fullname: Preynat-Seauve, Olivier – sequence: 7 givenname: Cecile surname: Guichard fullname: Guichard, Cecile – sequence: 8 givenname: Jack L surname: Arbiser fullname: Arbiser, Jack L – sequence: 9 givenname: Botond surname: Banfi fullname: Banfi, Botond – sequence: 10 givenname: Jean-Claude surname: Pache fullname: Pache, Jean-Claude – sequence: 11 givenname: Constance surname: Barazzone-Argiroffo fullname: Barazzone-Argiroffo, Constance – sequence: 12 givenname: Karl-Heinz surname: Krause fullname: Krause, Karl-Heinz
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/21391892$$D View this record in MEDLINE/PubMed
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References	18163953 - Cell Mol Immunol. 2007 Dec;4(6):419-29 16537427 - Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4604-9 17575013 - Am J Physiol Lung Cell Mol Physiol. 2007 Sep;293(3):L619-29 11252892 - Nat Rev Mol Cell Biol. 2000 Dec;1(3):169-78 16179589 - Circ Res. 2005 Oct 28;97(9):900-7 17635115 - Biochem Soc Trans. 2007 Aug;35(Pt 4):661-4 17729308 - J Cell Biochem. 2007 Oct 15;102(3):593-608 12060566 - Am J Physiol Lung Cell Mol Physiol. 2002 Jul;283(1):L103-12 15572675 - Mol Cell Biol. 2004 Dec;24(24):10703-17 9843857 - Am J Physiol. 1998 Dec;275(6 Pt 1):L1192-9 21072051 - Leukemia. 2011 Feb;25(2):281-9 16738200 - Proc Am Thorac Soc. 2006 Jun;3(4):350-6 18061509 - Int J Biochem Cell Biol. 2008;40(3):383-408 16306527 - N Engl J Med. 2005 Nov 24;353(21):2285-7 18161745 - J Pathol. 2008 Jan;214(2):199-210 17501721 - Biochem J. 2007 Aug 15;406(1):105-14 17237347 - Physiol Rev. 2007 Jan;87(1):245-313 18375206 - FEBS Lett. 2008 Jun 18;582(14):2051-65 17299435 - J Invest Dermatol. 2007 Mar;127(3):526-37 15289506 - J Exp Med. 2004 Aug 2;200(3):377-89 17537563 - Biochimie. 2007 Sep;89(9):1113-22 19779036 - Endocr Relat Cancer. 2010 Mar;17(1):27-37 20685750 - Thorax. 2010 Aug;65(8):733-8 19701206 - Nat Med. 2009 Sep;15(9):1077-81 16306520 - N Engl J Med. 2005 Nov 24;353(21):2229-42 17209037 - J Biol Chem. 2007 Mar 9;282(10):7723-32 17343348 - J Am Assoc Lab Anim Sci. 2007 Mar;46(2):21-4 8756825 - Am J Respir Crit Care Med. 1996 Aug;154(2 Pt 1):477-83 21217672 - Nat Med. 2011 Jan;17(1):31-2; author reply 32-3 19661248 - Am J Respir Crit Care Med. 2009 Nov 15;180(10):972-81 12746254 - Am J Respir Crit Care Med. 2003 Aug 15;168(4):431-5 10869423 - Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):8010-4 19850947 - Am J Respir Crit Care Med. 2010 Feb 1;181(3):254-63 17961070 - Antioxid Redox Signal. 2008 Feb;10(2):333-42 20942471 - J Med Chem. 2010 Nov 11;53(21):7715-30 19628035 - Free Radic Biol Med. 2009 Nov 1;47(9):1239-53 17993587 - Am J Physiol Lung Cell Mol Physiol. 2008 Feb;294(2):L152-60 19620773 - J Clin Invest. 2009 Aug;119(8):2359-65 11988769 - Nat Rev Mol Cell Biol. 2002 May;3(5):349-63 3539945 - J Cell Biol. 1986 Dec;103(6 Pt 2):2787-96 11177318 - Ann Intern Med. 2001 Jan 16;134(2):136-51 10893213 - Am J Physiol Lung Cell Mol Physiol. 2000 Jul;279(1):L143-51 15857893 - FASEB J. 2005 May;19(7):854-6 15663794 - Respir Res. 2005;6:11 15894605 - Am J Respir Crit Care Med. 2005 Aug 15;172(4):417-22 18836136 - Am J Respir Cell Mol Biol. 2009 Apr;40(4):422-32 17999627 - Antioxid Redox Signal. 2008 Feb;10(2):355-70 17936056 - Int J Biochem Cell Biol. 2008;40(3):362-82 8600933 - Am J Respir Cell Mol Biol. 1996 Apr;14(4):309-15
References_xml	– reference: 12746254 - Am J Respir Crit Care Med. 2003 Aug 15;168(4):431-5 – reference: 20942471 - J Med Chem. 2010 Nov 11;53(21):7715-30 – reference: 17936056 - Int J Biochem Cell Biol. 2008;40(3):362-82 – reference: 16738200 - Proc Am Thorac Soc. 2006 Jun;3(4):350-6 – reference: 17999627 - Antioxid Redox Signal. 2008 Feb;10(2):355-70 – reference: 17993587 - Am J Physiol Lung Cell Mol Physiol. 2008 Feb;294(2):L152-60 – reference: 19628035 - Free Radic Biol Med. 2009 Nov 1;47(9):1239-53 – reference: 16537427 - Proc Natl Acad Sci U S A. 2006 Mar 21;103(12):4604-9 – reference: 19779036 - Endocr Relat Cancer. 2010 Mar;17(1):27-37 – reference: 20685750 - Thorax. 2010 Aug;65(8):733-8 – reference: 15894605 - Am J Respir Crit Care Med. 2005 Aug 15;172(4):417-22 – reference: 21072051 - Leukemia. 2011 Feb;25(2):281-9 – reference: 21217672 - Nat Med. 2011 Jan;17(1):31-2; author reply 32-3 – reference: 18836136 - Am J Respir Cell Mol Biol. 2009 Apr;40(4):422-32 – reference: 16306520 - N Engl J Med. 2005 Nov 24;353(21):2229-42 – reference: 17729308 - J Cell Biochem. 2007 Oct 15;102(3):593-608 – reference: 19850947 - Am J Respir Crit Care Med. 2010 Feb 1;181(3):254-63 – reference: 19661248 - Am J Respir Crit Care Med. 2009 Nov 15;180(10):972-81 – reference: 10869423 - Proc Natl Acad Sci U S A. 2000 Jul 5;97(14):8010-4 – reference: 16179589 - Circ Res. 2005 Oct 28;97(9):900-7 – reference: 12060566 - Am J Physiol Lung Cell Mol Physiol. 2002 Jul;283(1):L103-12 – reference: 15663794 - Respir Res. 2005;6:11 – reference: 11177318 - Ann Intern Med. 2001 Jan 16;134(2):136-51 – reference: 18163953 - Cell Mol Immunol. 2007 Dec;4(6):419-29 – reference: 11252892 - Nat Rev Mol Cell Biol. 2000 Dec;1(3):169-78 – reference: 8600933 - Am J Respir Cell Mol Biol. 1996 Apr;14(4):309-15 – reference: 17343348 - J Am Assoc Lab Anim Sci. 2007 Mar;46(2):21-4 – reference: 19701206 - Nat Med. 2009 Sep;15(9):1077-81 – reference: 17501721 - Biochem J. 2007 Aug 15;406(1):105-14 – reference: 9843857 - Am J Physiol. 1998 Dec;275(6 Pt 1):L1192-9 – reference: 16306527 - N Engl J Med. 2005 Nov 24;353(21):2285-7 – reference: 18061509 - Int J Biochem Cell Biol. 2008;40(3):383-408 – reference: 11988769 - Nat Rev Mol Cell Biol. 2002 May;3(5):349-63 – reference: 15289506 - J Exp Med. 2004 Aug 2;200(3):377-89 – reference: 15572675 - Mol Cell Biol. 2004 Dec;24(24):10703-17 – reference: 8756825 - Am J Respir Crit Care Med. 1996 Aug;154(2 Pt 1):477-83 – reference: 15857893 - FASEB J. 2005 May;19(7):854-6 – reference: 17209037 - J Biol Chem. 2007 Mar 9;282(10):7723-32 – reference: 17635115 - Biochem Soc Trans. 2007 Aug;35(Pt 4):661-4 – reference: 3539945 - J Cell Biol. 1986 Dec;103(6 Pt 2):2787-96 – reference: 17237347 - Physiol Rev. 2007 Jan;87(1):245-313 – reference: 17299435 - J Invest Dermatol. 2007 Mar;127(3):526-37 – reference: 10893213 - Am J Physiol Lung Cell Mol Physiol. 2000 Jul;279(1):L143-51 – reference: 17961070 - Antioxid Redox Signal. 2008 Feb;10(2):333-42 – reference: 18375206 - FEBS Lett. 2008 Jun 18;582(14):2051-65 – reference: 17537563 - Biochimie. 2007 Sep;89(9):1113-22 – reference: 18161745 - J Pathol. 2008 Jan;214(2):199-210 – reference: 19620773 - J Clin Invest. 2009 Aug;119(8):2359-65 – reference: 17575013 - Am J Physiol Lung Cell Mol Physiol. 2007 Sep;293(3):L619-29
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Snippet	The pathogenesis of pulmonary fibrosis is linked to oxidative stress, possibly generated by the reactive oxygen species (ROS) generating NADPH oxidase NOX4....
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SubjectTerms	Animals Apoptosis - drug effects Apoptosis - genetics Bleomycin - pharmacology Cells, Cultured Gene Expression Idiopathic Pulmonary Fibrosis - genetics Idiopathic Pulmonary Fibrosis - metabolism Idiopathic Pulmonary Fibrosis - pathology Male Mice NADPH Oxidase 4 NADPH Oxidases - antagonists & inhibitors NADPH Oxidases - genetics NADPH Oxidases - metabolism Oxidative Stress - genetics Pulmonary Alveoli - drug effects Pulmonary Alveoli - metabolism Pulmonary Alveoli - pathology Reactive Oxygen Species - metabolism Respiratory Mucosa - metabolism Respiratory Mucosa - pathology RNA, Small Interfering - genetics Smad2 Protein - metabolism Transforming Growth Factor beta1 - metabolism
Title	A key role for NOX4 in epithelial cell death during development of lung fibrosis
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