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Conference Paper: Paracrine effect of human mesenchymal stem cell on cigarette smoke medium-exposed human AC16 cardiomyocytes

TitleParacrine effect of human mesenchymal stem cell on cigarette smoke medium-exposed human AC16 cardiomyocytes
Authors
Issue Date2016
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 21st Medical Research Conference (MRC 2016), Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2016. In Hong Kong Medical Journal, 2016, v. 22 n. suppl.1, p. 40, abstract no. 61 How to Cite?
AbstractINTRODUCTION: Cigarette smoking is the major risk factor for cardiovascular disease (CVD). Mesenchymal stem cells (MSCs) are emerging as a promising therapeutic agent for tissue regeneration, especially in CVD. The biologically active molecules secreted from MSCs have been found to exert the paracrine actions in many processes of cardiac repair, including cardiac regeneration, neovascularisation, inflammation, apoptosis, remodelling, contractility, and metabolism. The aim of this study was to investigate the effects of secretions from MSCs in a cigarette smoke medium (CSM)–exposed AC16 cardiomyocytes model in vitro. METHODS: The AC16 cardiomyocyte 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 medium consisting of 1% fetal bovine serum 24 hours before treatment. CSM and conditioned medium (CdM) from bone marrow–derived mesenchymal stem cell (BM-MSC) or induced pluripotent stem cell–derived mesenchymal stem cell (iPSC-MSC) were added into cells and incubated for 24 hours. RESULTS: CdM from iPSC-MSC had a superior effect than that from BM-MSC in attenuating CSM-induced reactive oxygen species production via the reversal of total antioxidant capacity, and enzyme activities of superoxide dismutase and catalase. CdM from iPSC-MSC but not from BM-MSC inhibited CSM-induced NF-ᵏB and p38 MAPK activation. Furthermore, CdM from iPSC-MSC inhibited cell apoptosis caused by CSM exposure along with significant reversal of Bax/Bcl-2 ratio. CONCLUSION: These data suggest that iPSC-MSCs mediate direct protective effects on cardiomyocytes by inhibiting cell injury through the paracrine action of unknown secretory factor with anti-oxidative and antiapoptotic properties, via the inhibition of NF-ᵏB and p38 MAPK signalling pathways in vitro.
Persistent Identifierhttp://hdl.handle.net/10722/234169
ISSN
2015 Impact Factor: 0.887
2015 SCImago Journal Rankings: 0.279

 

DC FieldValueLanguage
dc.contributor.authorLiang, YM-
dc.contributor.authorZhang, YL-
dc.contributor.authorIp, MSM-
dc.contributor.authorTse, HF-
dc.contributor.authorLian, Q-
dc.contributor.authorMak, JCW-
dc.date.accessioned2016-10-14T06:59:30Z-
dc.date.available2016-10-14T06:59:30Z-
dc.date.issued2016-
dc.identifier.citationThe 21st Medical Research Conference (MRC 2016), Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong, 16 January 2016. In Hong Kong Medical Journal, 2016, v. 22 n. suppl.1, p. 40, abstract no. 61-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/234169-
dc.description.abstractINTRODUCTION: Cigarette smoking is the major risk factor for cardiovascular disease (CVD). Mesenchymal stem cells (MSCs) are emerging as a promising therapeutic agent for tissue regeneration, especially in CVD. The biologically active molecules secreted from MSCs have been found to exert the paracrine actions in many processes of cardiac repair, including cardiac regeneration, neovascularisation, inflammation, apoptosis, remodelling, contractility, and metabolism. The aim of this study was to investigate the effects of secretions from MSCs in a cigarette smoke medium (CSM)–exposed AC16 cardiomyocytes model in vitro. METHODS: The AC16 cardiomyocyte 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 medium consisting of 1% fetal bovine serum 24 hours before treatment. CSM and conditioned medium (CdM) from bone marrow–derived mesenchymal stem cell (BM-MSC) or induced pluripotent stem cell–derived mesenchymal stem cell (iPSC-MSC) were added into cells and incubated for 24 hours. RESULTS: CdM from iPSC-MSC had a superior effect than that from BM-MSC in attenuating CSM-induced reactive oxygen species production via the reversal of total antioxidant capacity, and enzyme activities of superoxide dismutase and catalase. CdM from iPSC-MSC but not from BM-MSC inhibited CSM-induced NF-ᵏB and p38 MAPK activation. Furthermore, CdM from iPSC-MSC inhibited cell apoptosis caused by CSM exposure along with significant reversal of Bax/Bcl-2 ratio. CONCLUSION: These data suggest that iPSC-MSCs mediate direct protective effects on cardiomyocytes by inhibiting cell injury through the paracrine action of unknown secretory factor with anti-oxidative and antiapoptotic properties, via the inhibition of NF-ᵏB and p38 MAPK signalling pathways 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.titleParacrine effect of human mesenchymal stem cell on cigarette smoke medium-exposed human AC16 cardiomyocytes-
dc.typeConference_Paper-
dc.identifier.emailLiang, YM: winniell@hku.hk-
dc.identifier.emailZhang, YL: zyl1999@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailTse, HF: hftse@hkucc.hku.hk-
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityTse, HF=rp00428-
dc.identifier.authorityLian, Q=rp00267-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.hkuros267632-
dc.identifier.volume22-
dc.identifier.issuesuppl.1-
dc.identifier.spage40, abstract no. 61-
dc.identifier.epage40, abstract no. 61-
dc.publisher.placeHong Kong-

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