PMID- 29743070
OWN - NLM
STAT- MEDLINE
DCOM- 20181029
LR  - 20210826
IS  - 1465-993X (Electronic)
IS  - 1465-9921 (Print)
IS  - 1465-9921 (Linking)
VI  - 19
IP  - 1
DP  - 2018 May 9
TI  - The anti-proliferative and anti-inflammatory response of COPD airway smooth 
      muscle cells to hydrogen sulfide.
PG  - 85
LID - 10.1186/s12931-018-0788-x [doi]
LID - 85
AB  - 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-beta-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.
FAU - Perry, Mark M
AU  - Perry MM
AUID- ORCID: 0000-0002-8145-8042
AD  - School of Pharmacy & Biomedical Sciences, University of Portsmouth, St. Michael's 
      Building, White Swan Road, Portsmouth, PO1 2DT, UK. mark.perry@port.ac.uk.
FAU - Tildy, Bernadett
AU  - Tildy B
AD  - Airways Disease, National Heart and Lung Institute, Imperial College, London & 
      Royal Brompton NIHR Biomedical Research Unit, London, SW3 6LY, UK.
FAU - Papi, Alberto
AU  - Papi A
AD  - Sezione di Medicina Interna e Cardiorespiratoria, Centro Interdipartimentale per 
      lo Studio delle Malattie Infiammatorie delle Vie Aeree e Patologie Fumo-Correlate 
      (CEMICEF, formerly termed Centro di Ricerca su Asma e BPCO), Universita di 
      Ferrara, Ferrara, Italy.
FAU - Casolari, Paolo
AU  - Casolari P
AD  - Sezione di Medicina Interna e Cardiorespiratoria, Centro Interdipartimentale per 
      lo Studio delle Malattie Infiammatorie delle Vie Aeree e Patologie Fumo-Correlate 
      (CEMICEF, formerly termed Centro di Ricerca su Asma e BPCO), Universita di 
      Ferrara, Ferrara, Italy.
FAU - Caramori, Gaetano
AU  - Caramori G
AD  - Unita Operativa Complessa di Pneumologia, Dipartimento di Scienze Biomediche, 
      Odontoiatriche e delle Immagini Morfologiche e Funzionali (BIOMORF), Universita 
      degli Studi di Messina, Messina, Italy.
FAU - Rempel, Karen Limbert
AU  - Rempel KL
AD  - Departments of Internal Medicine & Physiology, Respiratory Hospital, Sherbrook 
      Street, Winnipeg, MB, R3A 1R9, Canada.
FAU - Halayko, Andrew J
AU  - Halayko AJ
AD  - Departments of Internal Medicine & Physiology, Respiratory Hospital, Sherbrook 
      Street, Winnipeg, MB, R3A 1R9, Canada.
FAU - Adcock, Ian
AU  - Adcock I
AD  - Airways Disease, National Heart and Lung Institute, Imperial College, London & 
      Royal Brompton NIHR Biomedical Research Unit, London, SW3 6LY, UK.
FAU - Chung, Kian Fan
AU  - Chung KF
AD  - Airways Disease, National Heart and Lung Institute, Imperial College, London & 
      Royal Brompton NIHR Biomedical Research Unit, London, SW3 6LY, UK.
LA  - eng
GR  - Wellcome Trust/United Kingdom
GR  - 08/041/Asthma UK/International
GR  - 085935/Wellcome Trust/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Retracted Publication
DEP - 20180509
PL  - England
TA  - Respir Res
JT  - Respiratory research
JID - 101090633
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Inflammation Mediators)
RN  - YY9FVM7NSN (Hydrogen Sulfide)
SB  - IM
RIN - Respir Res. 2021 Aug 25;22(1):235. PMID: 34433461
MH  - Aged
MH  - Anti-Inflammatory Agents/*pharmacology/therapeutic use
MH  - Cell Proliferation/*drug effects/physiology
MH  - Cells, Cultured
MH  - Female
MH  - Humans
MH  - Hydrogen Sulfide/*pharmacology/therapeutic use
MH  - Inflammation Mediators/antagonists & inhibitors/metabolism
MH  - Male
MH  - Middle Aged
MH  - Myocytes, Smooth Muscle/*drug effects/*metabolism/pathology
MH  - Pulmonary Disease, Chronic Obstructive/drug therapy/*metabolism/pathology
PMC - PMC5944010
OTO - NOTNLM
OT  - Airway smooth muscle
OT  - COPD
OT  - CXCL8
OT  - Hydrogen sulfide
OT  - IL-6
OT  - Proliferation
COIS- The authors declare that they have no competing interests.
EDAT- 2018/05/11 06:00
MHDA- 2018/10/30 06:00
PMCR- 2018/05/09
CRDT- 2018/05/11 06:00
PHST- 2018/02/12 00:00 [received]
PHST- 2018/04/23 00:00 [accepted]
PHST- 2018/05/11 06:00 [entrez]
PHST- 2018/05/11 06:00 [pubmed]
PHST- 2018/10/30 06:00 [medline]
PHST- 2018/05/09 00:00 [pmc-release]
AID - 10.1186/s12931-018-0788-x [pii]
AID - 788 [pii]
AID - 10.1186/s12931-018-0788-x [doi]
PST - epublish
SO  - Respir Res. 2018 May 9;19(1):85. doi: 10.1186/s12931-018-0788-x.