The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide

Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated...
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Autor*in:	Perry, Mark M. [verfasserIn] Tildy, Bernadett Papi, Alberto Casolari, Paolo Caramori, Gaetano Rempel, Karen Limbert Halayko, Andrew J. Adcock, Ian Chung, Kian Fan

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2018

Schlagwörter:	COPD Hydrogen sulfide Proliferation IL-6 CXCL8 Airway smooth muscle

Anmerkung:	© The Author(s). 2018

Übergeordnetes Werk:	Enthalten in: Respiratory research - London : BioMed Central, 2001, 19(2018), 1 vom: 09. Mai
Übergeordnetes Werk:	volume:19 ; year:2018 ; number:1 ; day:09 ; month:05

Links:	Volltext

DOI / URN:	10.1186/s12931-018-0788-x

Katalog-ID:	SPR028525485

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520			\|a Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production.
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700	1		\|a Chung, Kian Fan \|4 aut
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allfields	10.1186/s12931-018-0788-x doi (DE-627)SPR028525485 (SPR)s12931-018-0788-x-e DE-627 ger DE-627 rakwb eng Perry, Mark M. verfasserin (orcid)0000-0002-8145-8042 aut The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. COPD (dpeaa)DE-He213 Hydrogen sulfide (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 CXCL8 (dpeaa)DE-He213 Airway smooth muscle (dpeaa)DE-He213 Tildy, Bernadett aut Papi, Alberto aut Casolari, Paolo aut Caramori, Gaetano aut Rempel, Karen Limbert aut Halayko, Andrew J. aut Adcock, Ian aut Chung, Kian Fan aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 09. Mai (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:09 month:05 https://dx.doi.org/10.1186/s12931-018-0788-x 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 19 2018 1 09 05
spelling	10.1186/s12931-018-0788-x doi (DE-627)SPR028525485 (SPR)s12931-018-0788-x-e DE-627 ger DE-627 rakwb eng Perry, Mark M. verfasserin (orcid)0000-0002-8145-8042 aut The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. COPD (dpeaa)DE-He213 Hydrogen sulfide (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 CXCL8 (dpeaa)DE-He213 Airway smooth muscle (dpeaa)DE-He213 Tildy, Bernadett aut Papi, Alberto aut Casolari, Paolo aut Caramori, Gaetano aut Rempel, Karen Limbert aut Halayko, Andrew J. aut Adcock, Ian aut Chung, Kian Fan aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 09. Mai (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:09 month:05 https://dx.doi.org/10.1186/s12931-018-0788-x 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 19 2018 1 09 05
allfields_unstemmed	10.1186/s12931-018-0788-x doi (DE-627)SPR028525485 (SPR)s12931-018-0788-x-e DE-627 ger DE-627 rakwb eng Perry, Mark M. verfasserin (orcid)0000-0002-8145-8042 aut The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. COPD (dpeaa)DE-He213 Hydrogen sulfide (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 CXCL8 (dpeaa)DE-He213 Airway smooth muscle (dpeaa)DE-He213 Tildy, Bernadett aut Papi, Alberto aut Casolari, Paolo aut Caramori, Gaetano aut Rempel, Karen Limbert aut Halayko, Andrew J. aut Adcock, Ian aut Chung, Kian Fan aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 09. Mai (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:09 month:05 https://dx.doi.org/10.1186/s12931-018-0788-x 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 19 2018 1 09 05
allfieldsGer	10.1186/s12931-018-0788-x doi (DE-627)SPR028525485 (SPR)s12931-018-0788-x-e DE-627 ger DE-627 rakwb eng Perry, Mark M. verfasserin (orcid)0000-0002-8145-8042 aut The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. COPD (dpeaa)DE-He213 Hydrogen sulfide (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 CXCL8 (dpeaa)DE-He213 Airway smooth muscle (dpeaa)DE-He213 Tildy, Bernadett aut Papi, Alberto aut Casolari, Paolo aut Caramori, Gaetano aut Rempel, Karen Limbert aut Halayko, Andrew J. aut Adcock, Ian aut Chung, Kian Fan aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 09. Mai (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:09 month:05 https://dx.doi.org/10.1186/s12931-018-0788-x 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 19 2018 1 09 05
allfieldsSound	10.1186/s12931-018-0788-x doi (DE-627)SPR028525485 (SPR)s12931-018-0788-x-e DE-627 ger DE-627 rakwb eng Perry, Mark M. verfasserin (orcid)0000-0002-8145-8042 aut The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s). 2018 Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. COPD (dpeaa)DE-He213 Hydrogen sulfide (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 CXCL8 (dpeaa)DE-He213 Airway smooth muscle (dpeaa)DE-He213 Tildy, Bernadett aut Papi, Alberto aut Casolari, Paolo aut Caramori, Gaetano aut Rempel, Karen Limbert aut Halayko, Andrew J. aut Adcock, Ian aut Chung, Kian Fan aut Enthalten in Respiratory research London : BioMed Central, 2001 19(2018), 1 vom: 09. Mai (DE-627)326646485 (DE-600)2041675-1 1465-993X nnns volume:19 year:2018 number:1 day:09 month:05 https://dx.doi.org/10.1186/s12931-018-0788-x 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 19 2018 1 09 05
language	English
source	Enthalten in Respiratory research 19(2018), 1 vom: 09. Mai volume:19 year:2018 number:1 day:09 month:05
sourceStr	Enthalten in Respiratory research 19(2018), 1 vom: 09. Mai volume:19 year:2018 number:1 day:09 month:05
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	COPD Hydrogen sulfide Proliferation IL-6 CXCL8 Airway smooth muscle
isfreeaccess_bool	true
container_title	Respiratory research
authorswithroles_txt_mv	Perry, Mark M. @@aut@@ Tildy, Bernadett @@aut@@ Papi, Alberto @@aut@@ Casolari, Paolo @@aut@@ Caramori, Gaetano @@aut@@ Rempel, Karen Limbert @@aut@@ Halayko, Andrew J. @@aut@@ Adcock, Ian @@aut@@ Chung, Kian Fan @@aut@@
publishDateDaySort_date	2018-05-09T00:00:00Z
hierarchy_top_id	326646485
id	SPR028525485
language_de	englisch
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Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. 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author	Perry, Mark M.
spellingShingle	Perry, Mark M. misc COPD misc Hydrogen sulfide misc Proliferation misc IL-6 misc CXCL8 misc Airway smooth muscle The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide
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topic_title	The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide COPD (dpeaa)DE-He213 Hydrogen sulfide (dpeaa)DE-He213 Proliferation (dpeaa)DE-He213 IL-6 (dpeaa)DE-He213 CXCL8 (dpeaa)DE-He213 Airway smooth muscle (dpeaa)DE-He213
topic	misc COPD misc Hydrogen sulfide misc Proliferation misc IL-6 misc CXCL8 misc Airway smooth muscle
topic_unstemmed	misc COPD misc Hydrogen sulfide misc Proliferation misc IL-6 misc CXCL8 misc Airway smooth muscle
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title	The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide
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title_full	The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide
author_sort	Perry, Mark M.
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author_browse	Perry, Mark M. Tildy, Bernadett Papi, Alberto Casolari, Paolo Caramori, Gaetano Rempel, Karen Limbert Halayko, Andrew J. Adcock, Ian Chung, Kian Fan
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title_sort	anti-proliferative and anti-inflammatory response of copd airway smooth muscle cells to hydrogen sulfide
title_auth	The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide
abstract	Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. © The Author(s). 2018
abstractGer	Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. © The Author(s). 2018
abstract_unstemmed	Backbround COPD is a common, highly debilitating disease of the airways, primarily caused by smoking. Chronic inflammation and structural remodelling are key pathological features of this disease caused, in part, by the aberrant function of airway smooth muscle (ASM). We have previously demonstrated that hydrogen sulfide ($ H_{2} $S) can inhibit ASM cell proliferation and CXCL8 release, from cells isolated from non-smokers. Methods We examined the effect of $ H_{2} $S upon ASM cells from COPD patients. ASM cells were isolated from non-smokers, smokers and patients with COPD (n = 9). Proliferation and cytokine release (IL-6 and CXCL8) of ASM was induced by FCS, and measured by bromodeoxyuridine incorporation and ELISA, respectively. Results Exposure of ASM to $ H_{2} $S donors inhibited FCS-induced proliferation and cytokine release, but was less effective upon COPD ASM cells compared to the non-smokers and smokers. The mRNA and protein expression of the enzymes responsible for endogenous $ H_{2} $S production (cystathionine-β-synthase [CBS] and 3-mercaptopyruvate sulphur transferase [MPST]) were inhibited by $ H_{2} $S donors. Finally, we report that exogenous $ H_{2} $S inhibited FCS-stimulated phosphorylation of ERK–1/2 and p38 mitogen activated protein kinases (MAPKs), in the non-smoker and smoker ASM cells, with little effect in COPD cells. Conclusions $ H_{2} $S production provides a novel mechanism for the repression of ASM proliferation and cytokine release. The ability of COPD ASM cells to respond to $ H_{2} $S is attenuated in COPD ASM cells despite the presence of the enzymes responsible for $ H_{2} $S production. © The Author(s). 2018
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title_short	The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide
url	https://dx.doi.org/10.1186/s12931-018-0788-x
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author2	Tildy, Bernadett Papi, Alberto Casolari, Paolo Caramori, Gaetano Rempel, Karen Limbert Halayko, Andrew J. Adcock, Ian Chung, Kian Fan
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up_date	2024-07-03T19:59:40.203Z
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The anti-proliferative and anti-inflammatory response of COPD airway smooth muscle cells to hydrogen sulfide

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