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Vascular proteomics reveal novel proteins involved in SMC phenotypic change: OLR1 as a SMC receptor regulating proliferation and inflammatory response

Title
Vascular proteomics reveal novel proteins involved in SMC phenotypic change: OLR1 as a SMC receptor regulating proliferation and inflammatory response
Authors
KangD.H.ChoiM.ChangS.LeeM.Y.D.J.K.ParkJ.HanE.C.HwangD.KwonJoH.C.S.W.
Ewha Authors
강상원권기환이두재강동훈
SCOPUS Author ID
강상원scopus; 권기환scopus; 이두재scopus; 강동훈scopus
Issue Date
2015
Journal Title
PLoS ONE
ISSN
1932-6203JCR Link
Citation
vol. 10, no. 8
Publisher
Public Library of Science
Indexed
SCIE; SCOPUS WOS scopus
Abstract
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.
DOI
10.1371/journal.pone.0133845
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자연과학대학 > 생명과학전공 > Journal papers
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