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Conference Paper: Oxidative stress-induced mitochondria alteration in human airway smooth muscle cells and mesenchymal stem cells

TitleOxidative stress-induced mitochondria alteration in human airway smooth muscle cells and mesenchymal stem cells
Authors
KeywordsMedical sciences
Respiratory diseases
Issue Date2015
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
The 2015 International Conference of the American Thoracic Society (ATS), Denver, CO., 15-20 May 2015. In American Journal of Respiratory and Critical Care Medicine, 2015, v. 191 meeting abstracts, p. A5544 How to Cite?
AbstractRATIONALE: Exposure to cigarette smoke (CS) is the primary cause of chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS) produced by CS, as well as by infiltrating inflammatory cells, in conjunction with compromised antioxidant defenses in the lungs of COPD patients, results in oxidative stress. Oxidative stress leads to defective function of lung cells, such as airway smooth muscle cells (ASMCs), driving airway inflammation and remodelling. Mitochondrial dysfunction caused by oxidative stress leads to changes in cell survival and inflammatory responses. Mitochondrial transfer between mesenchymal stem cell (MSC) and airway cells has been shown to reverse mitochondrial dysfunction in lung disease models. We investigated the effect of oxidative stress on mitochondrial function and viability of …
DescriptionPoster Discussion Session - D27. Mitochondria: Live and Let Die: no. A5544
Persistent Identifierhttp://hdl.handle.net/10722/212215
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832

 

DC FieldValueLanguage
dc.contributor.authorLi, X-
dc.contributor.authorMichaeloudes, C-
dc.contributor.authorZhang, Y-
dc.contributor.authorLian, Q-
dc.contributor.authorMak, JC-
dc.contributor.authorBhavsar, PK-
dc.contributor.authorChung, KF-
dc.date.accessioned2015-07-21T02:27:53Z-
dc.date.available2015-07-21T02:27:53Z-
dc.date.issued2015-
dc.identifier.citationThe 2015 International Conference of the American Thoracic Society (ATS), Denver, CO., 15-20 May 2015. In American Journal of Respiratory and Critical Care Medicine, 2015, v. 191 meeting abstracts, p. A5544-
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/212215-
dc.descriptionPoster Discussion Session - D27. Mitochondria: Live and Let Die: no. A5544-
dc.description.abstractRATIONALE: Exposure to cigarette smoke (CS) is the primary cause of chronic obstructive pulmonary disease (COPD). Reactive oxygen species (ROS) produced by CS, as well as by infiltrating inflammatory cells, in conjunction with compromised antioxidant defenses in the lungs of COPD patients, results in oxidative stress. Oxidative stress leads to defective function of lung cells, such as airway smooth muscle cells (ASMCs), driving airway inflammation and remodelling. Mitochondrial dysfunction caused by oxidative stress leads to changes in cell survival and inflammatory responses. Mitochondrial transfer between mesenchymal stem cell (MSC) and airway cells has been shown to reverse mitochondrial dysfunction in lung disease models. We investigated the effect of oxidative stress on mitochondrial function and viability of …-
dc.languageeng-
dc.publisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org-
dc.relation.ispartofAmerican Journal of Respiratory and Critical Care Medicine-
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectMedical sciences-
dc.subjectRespiratory diseases-
dc.titleOxidative stress-induced mitochondria alteration in human airway smooth muscle cells and mesenchymal stem cells-
dc.typeConference_Paper-
dc.identifier.emailZhang, Y: zyl1999@hku.hk-
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hk-
dc.identifier.emailMak, JC: judithmak@hku.hk-
dc.identifier.authorityLian, Q=rp00267-
dc.identifier.authorityMak, JC=rp00352-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1164/ajrccm-conference.2015.191.1_MeetingAbstracts.A5544-
dc.identifier.hkuros245918-
dc.identifier.hkuros264315-
dc.identifier.volume191-
dc.identifier.issuemeeting abstracts-
dc.identifier.spageA5544-
dc.identifier.epageA5544-
dc.publisher.placeUnited States-

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