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Conference Paper: Mitochondrial Transfer of Induced Pluripotent Stem Cell–Derived Mesenchymal Stem Cells to Airway Epithelial Cells Attenuates Cigarette Smoke–Induced Damage

TitleMitochondrial Transfer of Induced Pluripotent Stem Cell–Derived Mesenchymal Stem Cells to Airway Epithelial Cells Attenuates Cigarette Smoke–Induced Damage
Authors
Issue Date2014
PublisherAmerican Thoracic Society. The Journal's web site is located at http://ajrccm.atsjournals.org
Citation
The 2014 International Conference of the American Thoracic Society (ATS), San Diego, CA., 16-21 May 2014. In American Journal of Respiratory and Critical Care Medicine, 2014, v. 189, abstract no. A5295 How to Cite?
AbstractTransplantation of mesenchymal stem cells (MSCs) holds great promise in the repair of cigarette smoke (CS)-induced lung damage in chronic obstructive pulmonary disease (COPD). Because CS leads to mitochondrial dysfunction, we aimed to investigate the potential benefit of mitochondrial transfer from human-induced pluripotent stem cell–derived MSCs (iPSC-MSCs) to CS-exposed airway epithelial cells in vitro and in vivo. Rats were exposed to 4% CS for 1 hour daily for 56 days. At Days 29 and, human iPSC-MSCs or adult bone marrow–derived MSCs (BM-MSCs) were administered intravenously to CS-exposed rats. CS-exposed rats exhibited severe alveolar destruction with a higher mean linear intercept (Lm) than sham air–exposed rats (P < 0.001) that was attenuated in the presence of iPSC-MSCs or BM-MSCs (P < 0.01). The attenuation of Lm value and the severity of fibrosis was greater in the iPSC-MSC–treated group than in the BM-MSC–treated group (P < 0.05). This might have contributed to the novel observation of mitochondrial transfer from MSCs to rat airway epithelial cells in lung sections exposed to CS. In vitro studies further revealed that transfer of mitochondria from iPSC-MSCs to bronchial epithelial cells (BEAS-2B) was more effective than from BM-MSCs, with preservation of adenosine triphosphate contents. This distinct mitochondrial transfer occurred via the formation of tunneling nanotubes. Inhibition of tunneling nanotube formation blocked mitochondrial transfer. Our findings indicate a higher mitochondrial transfer capacity of iPSC-MSCs than BM-MSCs to rescue CS-induced mitochondrial damage. iPSC-MSCs may thus hold promise for the development of cell therapy in COPD. Read More: http://www.atsjournals.org/doi/abs/10.1165/rcmb.2013-0529OC#.VFyVL_mUd1Y
DescriptionPoster Discussion Session C108: Is There Anything They Can't Do? Diverse Functional Activities of Mesenchymal Stem and Stromal Cells
Persistent Identifierhttp://hdl.handle.net/10722/202100
ISSN
2015 Impact Factor: 13.118
2015 SCImago Journal Rankings: 5.832

 

DC FieldValueLanguage
dc.contributor.authorLi, Xen_US
dc.contributor.authorZhang, Yen_US
dc.contributor.authorLiang, Yen_US
dc.contributor.authorYeung, SCen_US
dc.contributor.authorIp, MSMen_US
dc.contributor.authorTse, HFen_US
dc.contributor.authorLian, Qen_US
dc.contributor.authorMak, JCWen_US
dc.date.accessioned2014-08-21T08:03:50Z-
dc.date.available2014-08-21T08:03:50Z-
dc.date.issued2014en_US
dc.identifier.citationThe 2014 International Conference of the American Thoracic Society (ATS), San Diego, CA., 16-21 May 2014. In American Journal of Respiratory and Critical Care Medicine, 2014, v. 189, abstract no. A5295en_US
dc.identifier.issn1073-449X-
dc.identifier.urihttp://hdl.handle.net/10722/202100-
dc.descriptionPoster Discussion Session C108: Is There Anything They Can't Do? Diverse Functional Activities of Mesenchymal Stem and Stromal Cells-
dc.description.abstractTransplantation of mesenchymal stem cells (MSCs) holds great promise in the repair of cigarette smoke (CS)-induced lung damage in chronic obstructive pulmonary disease (COPD). Because CS leads to mitochondrial dysfunction, we aimed to investigate the potential benefit of mitochondrial transfer from human-induced pluripotent stem cell–derived MSCs (iPSC-MSCs) to CS-exposed airway epithelial cells in vitro and in vivo. Rats were exposed to 4% CS for 1 hour daily for 56 days. At Days 29 and, human iPSC-MSCs or adult bone marrow–derived MSCs (BM-MSCs) were administered intravenously to CS-exposed rats. CS-exposed rats exhibited severe alveolar destruction with a higher mean linear intercept (Lm) than sham air–exposed rats (P < 0.001) that was attenuated in the presence of iPSC-MSCs or BM-MSCs (P < 0.01). The attenuation of Lm value and the severity of fibrosis was greater in the iPSC-MSC–treated group than in the BM-MSC–treated group (P < 0.05). This might have contributed to the novel observation of mitochondrial transfer from MSCs to rat airway epithelial cells in lung sections exposed to CS. In vitro studies further revealed that transfer of mitochondria from iPSC-MSCs to bronchial epithelial cells (BEAS-2B) was more effective than from BM-MSCs, with preservation of adenosine triphosphate contents. This distinct mitochondrial transfer occurred via the formation of tunneling nanotubes. Inhibition of tunneling nanotube formation blocked mitochondrial transfer. Our findings indicate a higher mitochondrial transfer capacity of iPSC-MSCs than BM-MSCs to rescue CS-induced mitochondrial damage. iPSC-MSCs may thus hold promise for the development of cell therapy in COPD. Read More: http://www.atsjournals.org/doi/abs/10.1165/rcmb.2013-0529OC#.VFyVL_mUd1Y-
dc.languageengen_US
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 Medicineen_US
dc.titleMitochondrial Transfer of Induced Pluripotent Stem Cell–Derived Mesenchymal Stem Cells to Airway Epithelial Cells Attenuates Cigarette Smoke–Induced Damageen_US
dc.typeConference_Paperen_US
dc.identifier.emailYeung, SC: flag@hkucc.hku.hken_US
dc.identifier.emailIp, MSM: msmip@hku.hken_US
dc.identifier.emailTse, HF: hftse@hkucc.hku.hken_US
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hken_US
dc.identifier.emailMak, JCW: judithmak@hku.hken_US
dc.identifier.authorityIp, MSM=rp00347en_US
dc.identifier.authorityTse, HF=rp00428en_US
dc.identifier.authorityLian, Q=rp00267en_US
dc.identifier.authorityMak, JCW=rp00352en_US
dc.identifier.hkuros234872en_US
dc.identifier.volume189en_US
dc.publisher.placeUnited States-

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