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Article: Overexpression of ERBB4 rejuvenates aged mesenchymal stem cells and enhances angiogenesis via PI3K/AKT and MAPK/ERK pathways

TitleOverexpression of ERBB4 rejuvenates aged mesenchymal stem cells and enhances angiogenesis via PI3K/AKT and MAPK/ERK pathways
Authors
KeywordsMSC
Aging
Myocardial infarction
Issue Date2019
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
The FASEB Journal, 2019, v. 33 n. 3, p. 4559-4570 How to Cite?
AbstractThe age-related functional exhaustion limits potential efficacy of mesenchymal stem cells (MSC) in treating cardiovascular disease. Therefore, rejuvenation of aged MSC in the elderly population is of great interest. We have previously reported that Erb-B2 receptor tyrosine kinase 4 (ERBB4) plays a critical role in regulating MSC survival under hypoxia. The aim of this study was to investigate whether ERBB4 rejuvenates aged MSC and how ERBB4 enhances therapeutic efficacy of aged MSC in treating myocardial infarction (MI). Compared with vector aged MSC (aged-MSC), ERBB4-engineered aged MSC (ER4-aged-MSC) conferred resistance to oxidative stress-induced cell death and ameliorated the senescent phenotype in vitro. Four weeks after MI, the ER4-aged-MSC group exhibited enhanced blood vessel density, reduced cardiac remodeling and apoptosis with improved heart function compared with the aged-MSC group. Overexpression of ERBB4 caused an increase in phosphorylated v-akt murine thymoma viral oncogene homolog 1 (AKT), and phosphorylated ERK expression under hypoxia. ER4-aged-MSC secreted higher levels of angiopoietin, epithelial neutrophil activating peptide 78, VEGF, and fibroblast growth factor 2, and enhanced tube formation in HUVEC. The impact of ERBB4 on protein expression, proangiogenesis, cell behavior, and cytokine secretion was abolished by inhibiting PI3K/AKT and MAPK/ERK signaling pathway.
Persistent Identifierhttp://hdl.handle.net/10722/269441
ISSN
2017 Impact Factor: 5.595
2015 SCImago Journal Rankings: 2.775
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLiang, X-
dc.contributor.authorDing, Y-
dc.contributor.authorLin, F-
dc.contributor.authorZhang, Y-
dc.contributor.authorZhou, X-
dc.contributor.authorMeng, Q-
dc.contributor.authorLu, X-
dc.contributor.authorJiang, G-
dc.contributor.authorZhu, H-
dc.contributor.authorChen, Y-
dc.contributor.authorLian, Q-
dc.contributor.authorFan, H-
dc.contributor.authorLiu, Z-
dc.date.accessioned2019-04-24T08:07:47Z-
dc.date.available2019-04-24T08:07:47Z-
dc.date.issued2019-
dc.identifier.citationThe FASEB Journal, 2019, v. 33 n. 3, p. 4559-4570-
dc.identifier.issn0892-6638-
dc.identifier.urihttp://hdl.handle.net/10722/269441-
dc.description.abstractThe age-related functional exhaustion limits potential efficacy of mesenchymal stem cells (MSC) in treating cardiovascular disease. Therefore, rejuvenation of aged MSC in the elderly population is of great interest. We have previously reported that Erb-B2 receptor tyrosine kinase 4 (ERBB4) plays a critical role in regulating MSC survival under hypoxia. The aim of this study was to investigate whether ERBB4 rejuvenates aged MSC and how ERBB4 enhances therapeutic efficacy of aged MSC in treating myocardial infarction (MI). Compared with vector aged MSC (aged-MSC), ERBB4-engineered aged MSC (ER4-aged-MSC) conferred resistance to oxidative stress-induced cell death and ameliorated the senescent phenotype in vitro. Four weeks after MI, the ER4-aged-MSC group exhibited enhanced blood vessel density, reduced cardiac remodeling and apoptosis with improved heart function compared with the aged-MSC group. Overexpression of ERBB4 caused an increase in phosphorylated v-akt murine thymoma viral oncogene homolog 1 (AKT), and phosphorylated ERK expression under hypoxia. ER4-aged-MSC secreted higher levels of angiopoietin, epithelial neutrophil activating peptide 78, VEGF, and fibroblast growth factor 2, and enhanced tube formation in HUVEC. The impact of ERBB4 on protein expression, proangiogenesis, cell behavior, and cytokine secretion was abolished by inhibiting PI3K/AKT and MAPK/ERK signaling pathway.-
dc.languageeng-
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/-
dc.relation.ispartofThe FASEB Journal-
dc.subjectMSC-
dc.subjectAging-
dc.subjectMyocardial infarction-
dc.titleOverexpression of ERBB4 rejuvenates aged mesenchymal stem cells and enhances angiogenesis via PI3K/AKT and MAPK/ERK pathways-
dc.typeArticle-
dc.identifier.emailZhang, Y: zhangyuelin1999@163.com-
dc.identifier.emailLian, Q: qzlian@hkucc.hku.hk-
dc.identifier.authorityLian, Q=rp00267-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1096/fj.201801690R-
dc.identifier.pmid30566395-
dc.identifier.hkuros297521-
dc.identifier.volume33-
dc.identifier.issue3-
dc.identifier.spage4559-
dc.identifier.epage4570-
dc.identifier.isiWOS:000459794800116-
dc.publisher.placeUnited States-

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