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Article: Over-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway

TitleOver-expression of PDGFR-β promotes PDGF-induced proliferation, migration, and angiogenesis of EPCs through PI3K/Akt signaling pathway
Authors
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
PLoS One, 2012, v. 7 n. 2 How to Cite?
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-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.
Persistent Identifierhttp://hdl.handle.net/10722/168607
ISSN
2013 Impact Factor: 3.534
2013 SCImago Journal Rankings: 1.724
ISI Accession Number ID
References

 

Author Affiliations
  1. Third Military Medical University
DC FieldValueLanguage
dc.contributor.authorWang, Hen_US
dc.contributor.authorYin, Yen_US
dc.contributor.authorLi, Wen_US
dc.contributor.authorZhao, Xen_US
dc.contributor.authorYu, Yen_US
dc.contributor.authorZhu, Jen_US
dc.contributor.authorQin, Zen_US
dc.contributor.authorWang, Qen_US
dc.contributor.authorWang, Ken_US
dc.contributor.authorLu, Wen_US
dc.contributor.authorLiu, Jen_US
dc.contributor.authorHuang, Len_US
dc.date.accessioned2012-10-08T03:21:29Z-
dc.date.available2012-10-08T03:21:29Z-
dc.date.issued2012en_US
dc.identifier.citationPLoS One, 2012, v. 7 n. 2en_US
dc.identifier.issn1932-6203en_US
dc.identifier.urihttp://hdl.handle.net/10722/168607-
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.en_US
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_US
dc.relation.ispartofPLoS ONEen_US
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 pathwayen_US
dc.typeArticleen_US
dc.identifier.emailLu, W:luwei@hku.hken_US
dc.identifier.authorityLu, W=rp00754en_US
dc.description.naturepublished_or_final_versionen_US
dc.identifier.doi10.1371/journal.pone.0030503en_US
dc.identifier.pmid22355314-
dc.identifier.scopuseid_2-s2.0-84857080131en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84857080131&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume7en_US
dc.identifier.issue2en_US
dc.identifier.isiWOS:000302741300014-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridWang, H=54993293300en_US
dc.identifier.scopusauthoridYin, Y=54994935300en_US
dc.identifier.scopusauthoridLi, W=54992085900en_US
dc.identifier.scopusauthoridZhao, X=54991119200en_US
dc.identifier.scopusauthoridYu, Y=34979429100en_US
dc.identifier.scopusauthoridZhu, J=54993766300en_US
dc.identifier.scopusauthoridQin, Z=35211223400en_US
dc.identifier.scopusauthoridWang, Q=54991952200en_US
dc.identifier.scopusauthoridWang, K=54992506800en_US
dc.identifier.scopusauthoridLu, W=27868087600en_US
dc.identifier.scopusauthoridLiu, J=54993503300en_US
dc.identifier.scopusauthoridHuang, L=34769889600en_US

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