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Conference Paper: Involvement of MAPK and AMPK signaling pathways in cigarette smoke-induced inflammation in human AC16 cardiomyocytes

TitleInvolvement of MAPK and AMPK signaling pathways in cigarette smoke-induced inflammation in human AC16 cardiomyocytes
Authors
Issue Date2015
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 20th Medical Research Conference (MRC 2015), The University of Hong Kong, Hong Kong, 17 January 2015. In Hong Kong Medical Journal, 2015, v. 21 n. 1 suppl., p. 40, abstract no. 60 How to Cite?
AbstractINTRODUCTION: Cigarette smoke (CS) is the major risk factor of cardiovascular diseases. There is increasing evidence showing oxidative stress and inflammatory responses may play roles in the pathophysiological process; however, the underlying mechanism on CS-induced inflammation is currently unclear. The aim of this study was to investigate whether mitogen-activated protein kinase (MAPK) and AMP-activated protein kinase (AMPK) signalling pathways are involved in CS-induced inflammatory responses in human AC16 cardiomyocytes in vitro. METHODS: The AC16 cell line was cultured in DMEM/F12 containing 12.5% fetal bovine serum, in a CO2 incubator at 37°C. When cells reached 70% confluence, the medium was replaced with a medium consisting of 1% fetal bovine serum 24 hours before treatment. Cigarette smoke medium (CSM) was prepared by bubbling smoke from two cigarettes into 20 mL serum-free medium, which was regarded as 100%. Cells were pretreated with MAPK pathway inhibitors including U0126 (an ERK1/2 inhibitor), SB203580 (a p38 inhibitor) and SP600125 (a JNK inhibitor) and AMPK inhibitor Compound C for 30 minutes before 2% CSM was added and incubated for an additional 24 hours. Supernatant was collected for determination of interleukin (IL)–8 and IL-6 by enzyme-linked immunosorbent assay. Cell lysates were collected for Western blot analysis. RESULTS: CSM caused dose-dependent elevation of IL-8 and reduction of IL-6 in the supernatant of cardiomyocytes. MAPK inhibitors attenuated CSM-induced elevation of IL-8 release but no effect on CSM induced reduction of IL-6 release. On the other hand, Compound C abolished both CSM-induced IL-8 elevation and IL-6 reduction. Furthermore, CSM increased protein expression of anti-oxidative stress enzyme heme oxygenase 1 (HO-1) and quinone oxidoreductase 1 (NQO1), suggesting the existence of a defensive mechanism in cardiomyocytes. CONCLUSION: These findings suggest that MAPK but not AMPK have a differential role in controlling CSM induced IL-8 and IL-6 release via oxidative stress in human cardiomyoctyes in vitro.
Persistent Identifierhttp://hdl.handle.net/10722/232406
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorLiang, YM-
dc.contributor.authorIp, MSM-
dc.contributor.authorMak, JCW-
dc.date.accessioned2016-09-20T05:29:46Z-
dc.date.available2016-09-20T05:29:46Z-
dc.date.issued2015-
dc.identifier.citationThe 20th Medical Research Conference (MRC 2015), The University of Hong Kong, Hong Kong, 17 January 2015. In Hong Kong Medical Journal, 2015, v. 21 n. 1 suppl., p. 40, abstract no. 60-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/232406-
dc.description.abstractINTRODUCTION: Cigarette smoke (CS) is the major risk factor of cardiovascular diseases. There is increasing evidence showing oxidative stress and inflammatory responses may play roles in the pathophysiological process; however, the underlying mechanism on CS-induced inflammation is currently unclear. The aim of this study was to investigate whether mitogen-activated protein kinase (MAPK) and AMP-activated protein kinase (AMPK) signalling pathways are involved in CS-induced inflammatory responses in human AC16 cardiomyocytes in vitro. METHODS: The AC16 cell line was cultured in DMEM/F12 containing 12.5% fetal bovine serum, in a CO2 incubator at 37°C. When cells reached 70% confluence, the medium was replaced with a medium consisting of 1% fetal bovine serum 24 hours before treatment. Cigarette smoke medium (CSM) was prepared by bubbling smoke from two cigarettes into 20 mL serum-free medium, which was regarded as 100%. Cells were pretreated with MAPK pathway inhibitors including U0126 (an ERK1/2 inhibitor), SB203580 (a p38 inhibitor) and SP600125 (a JNK inhibitor) and AMPK inhibitor Compound C for 30 minutes before 2% CSM was added and incubated for an additional 24 hours. Supernatant was collected for determination of interleukin (IL)–8 and IL-6 by enzyme-linked immunosorbent assay. Cell lysates were collected for Western blot analysis. RESULTS: CSM caused dose-dependent elevation of IL-8 and reduction of IL-6 in the supernatant of cardiomyocytes. MAPK inhibitors attenuated CSM-induced elevation of IL-8 release but no effect on CSM induced reduction of IL-6 release. On the other hand, Compound C abolished both CSM-induced IL-8 elevation and IL-6 reduction. Furthermore, CSM increased protein expression of anti-oxidative stress enzyme heme oxygenase 1 (HO-1) and quinone oxidoreductase 1 (NQO1), suggesting the existence of a defensive mechanism in cardiomyocytes. CONCLUSION: These findings suggest that MAPK but not AMPK have a differential role in controlling CSM induced IL-8 and IL-6 release via oxidative stress in human cardiomyoctyes in vitro.-
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.titleInvolvement of MAPK and AMPK signaling pathways in cigarette smoke-induced inflammation in human AC16 cardiomyocytes-
dc.typeConference_Paper-
dc.identifier.emailLiang, YM: winniell@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.hkuros264309-
dc.identifier.volume21-
dc.identifier.issue1 suppl.-
dc.identifier.spage40, abstract no. 60-
dc.identifier.epage40, abstract no. 60-
dc.publisher.placeHong Kong-

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