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Article: Over-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway
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TitleOver-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway
 
AuthorsWang, H1
Yin, Y1
Li, W1
Zhao, X1
Yu, Y1
Zhu, J1
Qin, Z1
Wang, Q1
Wang, K1
Lu, W1
Liu, J1
Huang, L1
 
Issue Date2012
 
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
CitationPLoS One, 2012, v. 7 n. 2 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0030503
 
AbstractThe proliferation, migration, and angiogenesis of endothelial progenitor cells (EPCs) play critical roles in postnatal neovascularization and re-endothelialization following vascular injury. Here we evaluated whether the over-expression of platelet-derived growth factor receptor-β (PDGFR-β) can enhance the PDGF-BB-stimulated biological functions of EPCs through the PDGFR-β/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We first confirmed the expression of endogenous PDGFR-β and its plasma membrane localization in spleen-derived EPCs. We then demonstrated that the PDGFR-β over-expression in EPCs enhanced the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. Using AG1295 (a PDGFR kinase inhibitor), LY294002 (a PI3K inhibitor), and sc-221226 (an Akt inhibitor), we further showed that the PI3K/Akt signaling pathway participates in the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. In addition, the PI3K/Akt signaling pathway is required for PDGFR-β over-expression to enhance these PDGF-BB-induced phenotypes. © 2012 Wang et al.
 
ISSN1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
DOIhttp://dx.doi.org/10.1371/journal.pone.0030503
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorWang, H
 
dc.contributor.authorYin, Y
 
dc.contributor.authorLi, W
 
dc.contributor.authorZhao, X
 
dc.contributor.authorYu, Y
 
dc.contributor.authorZhu, J
 
dc.contributor.authorQin, Z
 
dc.contributor.authorWang, Q
 
dc.contributor.authorWang, K
 
dc.contributor.authorLu, W
 
dc.contributor.authorLiu, J
 
dc.contributor.authorHuang, L
 
dc.date.accessioned2012-10-08T03:21:29Z
 
dc.date.available2012-10-08T03:21:29Z
 
dc.date.issued2012
 
dc.description.abstractThe proliferation, migration, and angiogenesis of endothelial progenitor cells (EPCs) play critical roles in postnatal neovascularization and re-endothelialization following vascular injury. Here we evaluated whether the over-expression of platelet-derived growth factor receptor-β (PDGFR-β) can enhance the PDGF-BB-stimulated biological functions of EPCs through the PDGFR-β/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We first confirmed the expression of endogenous PDGFR-β and its plasma membrane localization in spleen-derived EPCs. We then demonstrated that the PDGFR-β over-expression in EPCs enhanced the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. Using AG1295 (a PDGFR kinase inhibitor), LY294002 (a PI3K inhibitor), and sc-221226 (an Akt inhibitor), we further showed that the PI3K/Akt signaling pathway participates in the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. In addition, the PI3K/Akt signaling pathway is required for PDGFR-β over-expression to enhance these PDGF-BB-induced phenotypes. © 2012 Wang et al.
 
dc.description.naturePublished_or_final_version
 
dc.identifier.citationPLoS One, 2012, v. 7 n. 2 [How to Cite?]
DOI: http://dx.doi.org/10.1371/journal.pone.0030503
 
dc.identifier.doihttp://dx.doi.org/10.1371/journal.pone.0030503
 
dc.identifier.issn1932-6203
2012 Impact Factor: 3.73
2012 SCImago Journal Rankings: 1.512
 
dc.identifier.issue2
 
dc.identifier.pmid22355314
 
dc.identifier.scopuseid_2-s2.0-84857080131
 
dc.identifier.urihttp://hdl.handle.net/10722/168607
 
dc.identifier.volume7
 
dc.languageeng
 
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
 
dc.publisher.placeUnited States
 
dc.relation.ispartofPLoS ONE
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.titleOver-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway
 
dc.typeArticle
 
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<contributor.author>Li, W</contributor.author>
<contributor.author>Zhao, X</contributor.author>
<contributor.author>Yu, Y</contributor.author>
<contributor.author>Zhu, J</contributor.author>
<contributor.author>Qin, Z</contributor.author>
<contributor.author>Wang, Q</contributor.author>
<contributor.author>Wang, K</contributor.author>
<contributor.author>Lu, W</contributor.author>
<contributor.author>Liu, J</contributor.author>
<contributor.author>Huang, L</contributor.author>
<date.accessioned>2012-10-08T03:21:29Z</date.accessioned>
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<description.abstract>The proliferation, migration, and angiogenesis of endothelial progenitor cells (EPCs) play critical roles in postnatal neovascularization and re-endothelialization following vascular injury. Here we evaluated whether the over-expression of platelet-derived growth factor receptor-&#946; (PDGFR-&#946;) can enhance the PDGF-BB-stimulated biological functions of EPCs through the PDGFR-&#946;/phosphoinositide 3-kinase (PI3K)/Akt signaling pathway. We first confirmed the expression of endogenous PDGFR-&#946; and its plasma membrane localization in spleen-derived EPCs. We then demonstrated that the PDGFR-&#946; over-expression in EPCs enhanced the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. Using AG1295 (a PDGFR kinase inhibitor), LY294002 (a PI3K inhibitor), and sc-221226 (an Akt inhibitor), we further showed that the PI3K/Akt signaling pathway participates in the PDGF-BB-induced proliferation, migration, and angiogenesis of EPCs. In addition, the PI3K/Akt signaling pathway is required for PDGFR-&#946; over-expression to enhance these PDGF-BB-induced phenotypes. &#169; 2012 Wang et al.</description.abstract>
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Author Affiliations
  1. Third Military Medical University