Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD

Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM )...
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Autor*in:	O'Leary, Lawrence [verfasserIn] Sevinç, Kenan Papazoglou, Ilektra M Tildy, Bernadett Detillieux, Karen Halayko, Andrew J Chung, Kian Fan Perry, Mark M

Format:	Artikel
Sprache:	Englisch

Erschienen:	2016

Rechteinformationen:	Nutzungsrecht: © 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies.

Schlagwörter:	inflammation RNA micro COPD

Übergeordnetes Werk:	Enthalten in: FEBS letters - Amsterdam [u.a.] : Elsevier, 1968, 590(2016), 9, Seite 1324-1334
Übergeordnetes Werk:	volume:590 ; year:2016 ; number:9 ; pages:1324-1334

Links:	Volltext Link aufrufen Link aufrufen

DOI / URN:	10.1002/1873-3468.12168

Katalog-ID:	OLC1974926311

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520			\|a Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 .
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700	1		\|a Chung, Kian Fan \|4 oth
700	1		\|a Perry, Mark M \|4 oth
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allfields	10.1002/1873-3468.12168 doi PQ20160719 (DE-627)OLC1974926311 (DE-599)GBVOLC1974926311 (PRQ)p948-1237757d858a5f8cd48b9a2f2885212d910351852cc61bc96e188315adc7f9500 (KEY)0045922420160000590000901324airwaysmoothmuscleinflammationisregulatedbymicrorn DE-627 ger DE-627 rakwb eng 570 530 610 DNB O'Leary, Lawrence verfasserin aut Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 . Nutzungsrecht: © 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. inflammation RNA micro COPD Sevinç, Kenan oth Papazoglou, Ilektra M oth Tildy, Bernadett oth Detillieux, Karen oth Halayko, Andrew J oth Chung, Kian Fan oth Perry, Mark M oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 590(2016), 9, Seite 1324-1334 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:590 year:2016 number:9 pages:1324-1334 http://dx.doi.org/10.1002/1873-3468.12168 Volltext http://onlinelibrary.wiley.com/doi/10.1002/1873-3468.12168/abstract http://www.ncbi.nlm.nih.gov/pubmed/27060571 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 AR 590 2016 9 1324-1334
spelling	10.1002/1873-3468.12168 doi PQ20160719 (DE-627)OLC1974926311 (DE-599)GBVOLC1974926311 (PRQ)p948-1237757d858a5f8cd48b9a2f2885212d910351852cc61bc96e188315adc7f9500 (KEY)0045922420160000590000901324airwaysmoothmuscleinflammationisregulatedbymicrorn DE-627 ger DE-627 rakwb eng 570 530 610 DNB O'Leary, Lawrence verfasserin aut Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 . Nutzungsrecht: © 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. inflammation RNA micro COPD Sevinç, Kenan oth Papazoglou, Ilektra M oth Tildy, Bernadett oth Detillieux, Karen oth Halayko, Andrew J oth Chung, Kian Fan oth Perry, Mark M oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 590(2016), 9, Seite 1324-1334 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:590 year:2016 number:9 pages:1324-1334 http://dx.doi.org/10.1002/1873-3468.12168 Volltext http://onlinelibrary.wiley.com/doi/10.1002/1873-3468.12168/abstract http://www.ncbi.nlm.nih.gov/pubmed/27060571 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 AR 590 2016 9 1324-1334
allfields_unstemmed	10.1002/1873-3468.12168 doi PQ20160719 (DE-627)OLC1974926311 (DE-599)GBVOLC1974926311 (PRQ)p948-1237757d858a5f8cd48b9a2f2885212d910351852cc61bc96e188315adc7f9500 (KEY)0045922420160000590000901324airwaysmoothmuscleinflammationisregulatedbymicrorn DE-627 ger DE-627 rakwb eng 570 530 610 DNB O'Leary, Lawrence verfasserin aut Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 . Nutzungsrecht: © 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. inflammation RNA micro COPD Sevinç, Kenan oth Papazoglou, Ilektra M oth Tildy, Bernadett oth Detillieux, Karen oth Halayko, Andrew J oth Chung, Kian Fan oth Perry, Mark M oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 590(2016), 9, Seite 1324-1334 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:590 year:2016 number:9 pages:1324-1334 http://dx.doi.org/10.1002/1873-3468.12168 Volltext http://onlinelibrary.wiley.com/doi/10.1002/1873-3468.12168/abstract http://www.ncbi.nlm.nih.gov/pubmed/27060571 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 AR 590 2016 9 1324-1334
allfieldsGer	10.1002/1873-3468.12168 doi PQ20160719 (DE-627)OLC1974926311 (DE-599)GBVOLC1974926311 (PRQ)p948-1237757d858a5f8cd48b9a2f2885212d910351852cc61bc96e188315adc7f9500 (KEY)0045922420160000590000901324airwaysmoothmuscleinflammationisregulatedbymicrorn DE-627 ger DE-627 rakwb eng 570 530 610 DNB O'Leary, Lawrence verfasserin aut Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 . Nutzungsrecht: © 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. inflammation RNA micro COPD Sevinç, Kenan oth Papazoglou, Ilektra M oth Tildy, Bernadett oth Detillieux, Karen oth Halayko, Andrew J oth Chung, Kian Fan oth Perry, Mark M oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 590(2016), 9, Seite 1324-1334 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:590 year:2016 number:9 pages:1324-1334 http://dx.doi.org/10.1002/1873-3468.12168 Volltext http://onlinelibrary.wiley.com/doi/10.1002/1873-3468.12168/abstract http://www.ncbi.nlm.nih.gov/pubmed/27060571 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 AR 590 2016 9 1324-1334
allfieldsSound	10.1002/1873-3468.12168 doi PQ20160719 (DE-627)OLC1974926311 (DE-599)GBVOLC1974926311 (PRQ)p948-1237757d858a5f8cd48b9a2f2885212d910351852cc61bc96e188315adc7f9500 (KEY)0045922420160000590000901324airwaysmoothmuscleinflammationisregulatedbymicrorn DE-627 ger DE-627 rakwb eng 570 530 610 DNB O'Leary, Lawrence verfasserin aut Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD 2016 Text txt rdacontent ohne Hilfsmittel zu benutzen n rdamedia Band nc rdacarrier Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 . Nutzungsrecht: © 2016 The Authors. FEBS Letters published by John Wiley & Sons Ltd on behalf of Federation of European Biochemical Societies. inflammation RNA micro COPD Sevinç, Kenan oth Papazoglou, Ilektra M oth Tildy, Bernadett oth Detillieux, Karen oth Halayko, Andrew J oth Chung, Kian Fan oth Perry, Mark M oth Enthalten in FEBS letters Amsterdam [u.a.] : Elsevier, 1968 590(2016), 9, Seite 1324-1334 (DE-627)129522023 (DE-600)212746-5 (DE-576)014938014 0014-5793 nnns volume:590 year:2016 number:9 pages:1324-1334 http://dx.doi.org/10.1002/1873-3468.12168 Volltext http://onlinelibrary.wiley.com/doi/10.1002/1873-3468.12168/abstract http://www.ncbi.nlm.nih.gov/pubmed/27060571 GBV_USEFLAG_A SYSFLAG_A GBV_OLC SSG-OLC-PHY SSG-OLC-CHE SSG-OLC-PHA SSG-OLC-DE-84 AR 590 2016 9 1324-1334
language	English
source	Enthalten in FEBS letters 590(2016), 9, Seite 1324-1334 volume:590 year:2016 number:9 pages:1324-1334
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title	Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD
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title_full	Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD
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title_sort	airway smooth muscle inflammation is regulated by microrna‐145 in copd
title_auth	Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD
abstract	Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 .
abstractGer	Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 .
abstract_unstemmed	Chronic obstructive pulmonary disease ( 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, in part caused by the aberrant function of airway smooth muscle ( ASM ) cells under the regulation of transforming growth factor ( TGF )‐β. miRNA are short, noncoding gene transcripts involved in the negative regulation of specific target genes, through their interactions with mRNA. Previous studies have proposed that mRNA‐145 ( miR‐145 ) may interact with SMAD 3 , an important downstream signalling molecule of the TGF ‐β pathway. TGF ‐β was used to stimulate primary human ASM cells isolated from healthy nonsmokers, healthy smokers and COPD patients. This resulted in a TGF ‐β‐dependent increase in CXCL 8 and IL ‐6 release, most notably in the cells from COPD patients. TGF ‐β stimulation increased SMAD 3 expression, only in cells from COPD patients, with a concurrent increased miR‐145 expression. Regulation of miR‐145 was found to be negatively controlled by pathways involving the MAP kinases, MEK ‐1/2 and p38 MAPK . Subsequent, overexpression of miR‐145 (using synthetic mimics) in ASM cells from patients with COPD suppressed IL ‐6 and CXCL 8 release, to levels comparable to the nonsmoker controls. Therefore, this study suggests that miR‐145 negatively regulates pro‐inflammatory cytokine release from ASM cells in COPD by targeting SMAD 3 .
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title_short	Airway smooth muscle inflammation is regulated by microRNA‐145 in COPD
url	http://dx.doi.org/10.1002/1873-3468.12168 http://onlinelibrary.wiley.com/doi/10.1002/1873-3468.12168/abstract http://www.ncbi.nlm.nih.gov/pubmed/27060571
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