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Conference Paper: Involvement of MAPK and AMPK signaling pathways in cigarette smoke-induced inflammation in human AC16 cardiomyocytes
Title | Involvement of MAPK and AMPK signaling pathways in cigarette smoke-induced inflammation in human AC16 cardiomyocytes |
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Authors | |
Issue Date | 2015 |
Publisher | Hong 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? |
Abstract | INTRODUCTION: 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 Identifier | http://hdl.handle.net/10722/232406 |
ISSN | 2023 Impact Factor: 3.1 2023 SCImago Journal Rankings: 0.261 |
DC Field | Value | Language |
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dc.contributor.author | Liang, YM | - |
dc.contributor.author | Ip, MSM | - |
dc.contributor.author | Mak, JCW | - |
dc.date.accessioned | 2016-09-20T05:29:46Z | - |
dc.date.available | 2016-09-20T05:29:46Z | - |
dc.date.issued | 2015 | - |
dc.identifier.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 | - |
dc.identifier.issn | 1024-2708 | - |
dc.identifier.uri | http://hdl.handle.net/10722/232406 | - |
dc.description.abstract | INTRODUCTION: 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.language | eng | - |
dc.publisher | Hong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/ | - |
dc.relation.ispartof | Hong Kong Medical Journal | - |
dc.rights | Hong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press. | - |
dc.title | Involvement of MAPK and AMPK signaling pathways in cigarette smoke-induced inflammation in human AC16 cardiomyocytes | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Liang, YM: winniell@hku.hk | - |
dc.identifier.email | Ip, MSM: msmip@hku.hk | - |
dc.identifier.email | Mak, JCW: judithmak@hku.hk | - |
dc.identifier.authority | Ip, MSM=rp00347 | - |
dc.identifier.authority | Mak, JCW=rp00352 | - |
dc.identifier.hkuros | 264309 | - |
dc.identifier.volume | 21 | - |
dc.identifier.issue | 1 suppl. | - |
dc.identifier.spage | 40, abstract no. 60 | - |
dc.identifier.epage | 40, abstract no. 60 | - |
dc.publisher.place | Hong Kong | - |
dc.identifier.issnl | 1024-2708 | - |