TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids
Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We s...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Doerner, Astrid M [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2009 |
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| Schlagwörter: |
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| Anmerkung: |
© Doerner and Zuraw. 2009 |
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| Übergeordnetes Werk: |
Enthalten in: Respiratory research - London : BioMed Central, 2001, 10(2009), 1 vom: 27. Okt. |
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| Übergeordnetes Werk: |
volume:10 ; year:2009 ; number:1 ; day:27 ; month:10 |
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| DOI / URN: |
10.1186/1465-9921-10-100 |
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| Katalog-ID: |
SPR028509625 |
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| 100 | 1 | |a Doerner, Astrid M |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids |
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| 520 | |a Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. | ||
| 650 | 4 | |a Idiopathic Pulmonary Fibrosis |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Budesonide |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Bronchial Epithelial Cell |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Airway Remodel |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a Human Bronchial Epithelial Cell |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Zuraw, Bruce L |4 aut | |
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2009 |
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10.1186/1465-9921-10-100 doi (DE-627)SPR028509625 (SPR)1465-9921-10-100-e DE-627 ger DE-627 rakwb eng Doerner, Astrid M verfasserin aut TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Doerner and Zuraw. 2009 Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. Idiopathic Pulmonary Fibrosis (dpeaa)DE-He213 Budesonide (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Human Bronchial Epithelial Cell (dpeaa)DE-He213 Zuraw, Bruce L aut Enthalten in Respiratory research London : BioMed Central, 2001 10(2009), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:10 year:2009 number:1 day:27 month:10 https://dx.doi.org/10.1186/1465-9921-10-100 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1 27 10 |
| spelling |
10.1186/1465-9921-10-100 doi (DE-627)SPR028509625 (SPR)1465-9921-10-100-e DE-627 ger DE-627 rakwb eng Doerner, Astrid M verfasserin aut TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Doerner and Zuraw. 2009 Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. Idiopathic Pulmonary Fibrosis (dpeaa)DE-He213 Budesonide (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Human Bronchial Epithelial Cell (dpeaa)DE-He213 Zuraw, Bruce L aut Enthalten in Respiratory research London : BioMed Central, 2001 10(2009), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:10 year:2009 number:1 day:27 month:10 https://dx.doi.org/10.1186/1465-9921-10-100 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1 27 10 |
| allfields_unstemmed |
10.1186/1465-9921-10-100 doi (DE-627)SPR028509625 (SPR)1465-9921-10-100-e DE-627 ger DE-627 rakwb eng Doerner, Astrid M verfasserin aut TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Doerner and Zuraw. 2009 Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. Idiopathic Pulmonary Fibrosis (dpeaa)DE-He213 Budesonide (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Human Bronchial Epithelial Cell (dpeaa)DE-He213 Zuraw, Bruce L aut Enthalten in Respiratory research London : BioMed Central, 2001 10(2009), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:10 year:2009 number:1 day:27 month:10 https://dx.doi.org/10.1186/1465-9921-10-100 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1 27 10 |
| allfieldsGer |
10.1186/1465-9921-10-100 doi (DE-627)SPR028509625 (SPR)1465-9921-10-100-e DE-627 ger DE-627 rakwb eng Doerner, Astrid M verfasserin aut TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Doerner and Zuraw. 2009 Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. Idiopathic Pulmonary Fibrosis (dpeaa)DE-He213 Budesonide (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Human Bronchial Epithelial Cell (dpeaa)DE-He213 Zuraw, Bruce L aut Enthalten in Respiratory research London : BioMed Central, 2001 10(2009), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:10 year:2009 number:1 day:27 month:10 https://dx.doi.org/10.1186/1465-9921-10-100 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1 27 10 |
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10.1186/1465-9921-10-100 doi (DE-627)SPR028509625 (SPR)1465-9921-10-100-e DE-627 ger DE-627 rakwb eng Doerner, Astrid M verfasserin aut TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Doerner and Zuraw. 2009 Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. Idiopathic Pulmonary Fibrosis (dpeaa)DE-He213 Budesonide (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Human Bronchial Epithelial Cell (dpeaa)DE-He213 Zuraw, Bruce L aut Enthalten in Respiratory research London : BioMed Central, 2001 10(2009), 1 vom: 27. Okt. (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:10 year:2009 number:1 day:27 month:10 https://dx.doi.org/10.1186/1465-9921-10-100 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2031 GBV_ILN_2038 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2061 GBV_ILN_2111 GBV_ILN_2113 GBV_ILN_2153 GBV_ILN_2190 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2009 1 27 10 |
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TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids Idiopathic Pulmonary Fibrosis (dpeaa)DE-He213 Budesonide (dpeaa)DE-He213 Bronchial Epithelial Cell (dpeaa)DE-He213 Airway Remodel (dpeaa)DE-He213 Human Bronchial Epithelial Cell (dpeaa)DE-He213 |
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Doerner, Astrid M |
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tgf-$ β_{1} $ induced epithelial to mesenchymal transition (emt) in human bronchial epithelial cells is enhanced by il-1β but not abrogated by corticosteroids |
| title_auth |
TGF-$ β_{1} $ induced epithelial to mesenchymal transition (EMT) in human bronchial epithelial cells is enhanced by IL-1β but not abrogated by corticosteroids |
| abstract |
Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. © Doerner and Zuraw. 2009 |
| abstractGer |
Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. © Doerner and Zuraw. 2009 |
| abstract_unstemmed |
Background Chronic persistent asthma is characterized by ongoing airway inflammation and airway remodeling. The processes leading to airway remodeling are poorly understood, and there is increasing evidence that even aggressive anti-inflammatory therapy does not completely prevent this process. We sought to investigate whether $ TGFβ_{1} $ stimulates bronchial epithelial cells to undergo transition to a mesenchymal phenotype, and whether this transition can be abrogated by corticosteroid treatment or enhanced by the pro-inflammatory cytokine IL-1β. Methods BEAS-2B and primary normal human bronchial epithelial cells were stimulated with $ TGFβ_{1} $ and expression of epithelial and mesenchymal markers assessed by quantitative real-time PCR, immunoblotting, immunofluorescence microscopy and zymography. In some cases the epithelial cells were also incubated with corticosteroids or IL-1β. Results were analyzed using non-parametric statistical tests. Results Treatment of BEAS-2B or primary human bronchial epithelial cells with $ TGFβ_{1} $ significantly reduced the expression level of the epithelial adherence junction protein E-cadherin. $ TGFβ_{1} $ then markedly induced mesenchymal marker proteins such as collagen I, tenascin C, fibronectin and α-smooth muscle actin mRNA in a dose dependant manner. The process of mesenchymal transition was accompanied by a morphological change towards a more spindle shaped fibroblast cell type with a more motile and invasive phenotype. Corticosteroid pre-treatment did not significantly alter the $ TGFβ_{1} $ induced transition but IL-1β enhanced the transition. Conclusion Our results indicate, that $ TGFβ_{1} $ can induce mesenchymal transition in the bronchial epithelial cell line and primary cells. Since asthma has been strongly associated with increased expression of $ TGFβ_{1} $ in the airway, epithelial to mesenchymal transition may contribute to the contractile and fibrotic remodeling process that accompanies chronic asthma. © Doerner and Zuraw. 2009 |
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