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Vascular Proteomics Reveal Novel Proteins Involved in SMC Phenotypic Change: OLR1 as a SMC Receptor Regulating Proliferation and Inflammatory Response

Vascular Proteomics Reveal Novel Proteins Involved in SMC Phenotypic Change: OLR1 as a SMC Receptor Regulating Proliferation and Inflammatory Response
Kang, Dong HoonChoi, MinaChang, SoyoungLee, Min YoungLee, Doo JaeChoi, KyungsunPark, JunseongHan, Eun ChunHwang, DaeheeKwon, KihwanJo, HanjoongChoi, ChulheeKang, Sang Won
DGIST Authors
Hwang, Daehee
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Article Type
AnimalAnimal ExperimentAnimal ModelAnimal TissueAnimalsArtery Intima ProliferationBiological ModelCarotid ArteriesCarotid ArteryCarotid Artery InjuryCell AdhesionCell MembraneCell MigrationCell ProliferationControlled StudyHumanHuman CellHumansHyperplasiaImmunoglobulin Enhancer Binding ProteinInflammationIntimal Thickness Related ReceptorMaleMetabolismModels, BiologicalMonocyteMuscle, Smooth, VascularMyocytes, Smooth MuscleNeointimaNon-HumanOldlr1 Protein, RatOLR1 Protein, HumanOxidized Low Density LipoproteinOxidized Low Density Lipoprotein ReceptorOxidized Low Density Lipoprotein Receptor 1PathologyPhenotypePhenotypic PlasticityPlatelet-Derived Growth FactorPlatelet-Derived Growth Factor Beta ReceptorProtein DNA InteractionProtein ExpressionProtein Interaction MapsProtein Protein InteractionProtein Tyrosine Phosphatase EpsilonProteomeProteomicsPyruvate DehydrogenasePyruvate Dehydrogenase BetaRab ProteinRab15 ProteinRatRats, Sprague-DawleyReceptors, Oxidized LDLRegulator ProteinScavenger Receptors, Class ESignal TransductionSmooth Muscle CellSprague Dawley RatU-937 Cell LineU-937 CellsUnclassified DrugVascular Smooth MuscleVascular Smooth Muscle Cell
Neointimal hyperplasia of vascular smooth muscle cells (VSMC) plays a critical role in atherosclerotic plaque formation and in-stent restenosis, but the underlying mechanisms are still incompletely understood. We performed a proteomics study to identify novel signaling molecules organizing the VSMC hyperplasia. The differential proteomics analysis in a balloon-induced injury model of rat carotid artery revealed that the expressions of 44 proteins are changed within 3 days post injury. The combination of cellular function assays and a protein network analysis further demonstrated that 27 out of 44 proteins constitute key signaling networks orchestrating the phenotypic change of VSMC from contractile to epitheliallike synthetic. Among the list of proteins, the in vivo validation specifically revealed that six proteins (Rab15, ITR, OLR1, PDHβ, PTPε) are positive regulators for VSMC hyperplasia. In particular, the OLR1 played dual roles in the VSMC hyperplasia by directly mediating oxidized LDL-induced monocyte adhesion via NF-êB activation and by assisting the PDGFinduced proliferation/migration. Importantly, OLR1 and PDGFRβ were associated in close proximity in the plasma membrane. Thus, this study elicits the protein network organizing the phenotypic change of VSMC in the vascular injury diseases such as atherosclerosis and discovers OLR1 as a novel molecular link between the proliferative and inflammatory responses of VSMCs. © 2015 Kang et al.
Public Library of Science
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Department of New Biology Systems Biology and Medicine Lab 1. Journal Articles


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