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Article: Connexin 43-Mediated Mitochondrial Transfer of iPSC-MSCs Alleviates Asthma Inflammation

TitleConnexin 43-Mediated Mitochondrial Transfer of iPSC-MSCs Alleviates Asthma Inflammation
Authors
KeywordsAsthma
Connexin 43
Epithelial cells
iPSC-MSCs
Mitochondrial transfer
Issue Date2018
PublisherElsevier (Cell Press): OAJ. The Journal's web site is located at http://stemcellreports.cell.com
Citation
Stem Cell Reports, 2018, v. 11 n. 5, p. 1120-1135 How to Cite?
AbstractWe previously identified an immunomodulatory role of human induced pluripotent stem cell (iPSC)-derived mesenchymal stem cells (MSCs) in asthmatic inflammation. Mitochondrial transfer from bone marrow MSCs to epithelial cells can result in the attenuation of acute lung injury in mice. However, the effects of mitochondrial transfer from iPSC-MSCs to epithelial cells in asthma and the mechanisms underlying these effects are unclear. We found that iPSC-MSC transplantation significantly reduced T helper 2 cytokines, attenuated the mitochondrial dysfunction of epithelial cells, and alleviated asthma inflammation in mice. Tunneling nanotubes (TNTs) were formed between iPSC-MSCs and epithelial cells, and mitochondrial transfer from iPSC-MSCs to epithelial cells via TNTs was observed both in vitro and in mice. Overexpression or silencing of connexin 43 (CX43) in iPSC-MSCs demonstrated that CX43 plays a critical role in the regulation of TNT formation by mediating mitochondrial transfer between iPSC-MSCs and epithelial cells. This study provides a therapeutic strategy for targeting asthma inflammation.
Persistent Identifierhttp://hdl.handle.net/10722/269387
ISSN
2023 Impact Factor: 5.9
2023 SCImago Journal Rankings: 2.518
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYao, Y-
dc.contributor.authorFan, XL-
dc.contributor.authorJiang, D-
dc.contributor.authorZhang, Y-
dc.contributor.authorLi, X-
dc.contributor.authorXu, ZB-
dc.contributor.authorFang, SB-
dc.contributor.authorChiu, S-
dc.contributor.authorTse, HF-
dc.contributor.authorLian, Q-
dc.contributor.authorFu, QL-
dc.date.accessioned2019-04-24T08:06:40Z-
dc.date.available2019-04-24T08:06:40Z-
dc.date.issued2018-
dc.identifier.citationStem Cell Reports, 2018, v. 11 n. 5, p. 1120-1135-
dc.identifier.issn2213-6711-
dc.identifier.urihttp://hdl.handle.net/10722/269387-
dc.description.abstractWe previously identified an immunomodulatory role of human induced pluripotent stem cell (iPSC)-derived mesenchymal stem cells (MSCs) in asthmatic inflammation. Mitochondrial transfer from bone marrow MSCs to epithelial cells can result in the attenuation of acute lung injury in mice. However, the effects of mitochondrial transfer from iPSC-MSCs to epithelial cells in asthma and the mechanisms underlying these effects are unclear. We found that iPSC-MSC transplantation significantly reduced T helper 2 cytokines, attenuated the mitochondrial dysfunction of epithelial cells, and alleviated asthma inflammation in mice. Tunneling nanotubes (TNTs) were formed between iPSC-MSCs and epithelial cells, and mitochondrial transfer from iPSC-MSCs to epithelial cells via TNTs was observed both in vitro and in mice. Overexpression or silencing of connexin 43 (CX43) in iPSC-MSCs demonstrated that CX43 plays a critical role in the regulation of TNT formation by mediating mitochondrial transfer between iPSC-MSCs and epithelial cells. This study provides a therapeutic strategy for targeting asthma inflammation.-
dc.languageeng-
dc.publisherElsevier (Cell Press): OAJ. The Journal's web site is located at http://stemcellreports.cell.com-
dc.relation.ispartofStem Cell Reports-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAsthma-
dc.subjectConnexin 43-
dc.subjectEpithelial cells-
dc.subjectiPSC-MSCs-
dc.subjectMitochondrial transfer-
dc.titleConnexin 43-Mediated Mitochondrial Transfer of iPSC-MSCs Alleviates Asthma Inflammation-
dc.typeArticle-
dc.identifier.emailZhang, Y: zhangyuelin1999@163.com-
dc.identifier.emailTse, HF: hftse@hkucc.hku.hk-
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hk-
dc.identifier.authorityTse, HF=rp00428-
dc.identifier.authorityLian, Q=rp00267-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1016/j.stemcr.2018.09.012-
dc.identifier.pmid30344008-
dc.identifier.pmcidPMC6234920-
dc.identifier.scopuseid_2-s2.0-85056655638-
dc.identifier.hkuros297520-
dc.identifier.volume11-
dc.identifier.issue5-
dc.identifier.spage1120-
dc.identifier.epage1135-
dc.identifier.isiWOS:000450127400010-
dc.publisher.placeUnited States-
dc.identifier.issnl2213-6711-

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