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
2011 Impact Factor: 4.092
2011 SCImago Journal Rankings: 0.519
DOIhttp://dx.doi.org/10.1371/journal.pone.0030503
ReferencesReferences in Scopus
DC Field
Value
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.natureLink_to_subscribed_fulltext
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
2011 Impact Factor: 4.092
2011 SCImago Journal Rankings: 0.519
dc.identifier.issue2
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.titleOver-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway
dc.typeArticle
Author Affiliations
  1. Third Military Medical University