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Wierer, M.* ; Prestel, M.* ; Schiller, H. B. ; Yan, G.* ; Schaab, C.* ; Azghandi, S.* ; Werner, J.* ; Kessler, T.* ; Malik, R.* ; Murgia, M.* ; Aherrahrou, Z.* ; Schunkert, H.* ; Dichgans, M.* ; Mann, M.*

Compartment-resolved proteomic analysis of mouse aorta during atherosclerotic plaque formation reveals osteoclast-specific protein expression.

Mol. Cell. Proteomics 17, 321-334 (2017)
Verlagsversion Postprint Forschungsdaten DOI
Open Access Green
Atherosclerosis leads to vascular lesions that involve major rearrangements of the vascular proteome, especially of the extracellular matrix (ECM). Using single aortas from ApoE knock out mice, we quantified formation of plaques by single-run, high-resolution mass spectrometry (MS)based proteomics. To probe localization on a proteome-wide scale we employed quantitative detergent solubility profiling. This compartment- and time-resolved resource of atherogenesis comprised 5117 proteins, 182 of which changed their expression status in response to vessel maturation and atherosclerotic plaque development. In the insoluble ECM proteome, 65 proteins significantly changed, including relevant collagens, matrix metalloproteinases and macrophage derived proteins. Among novel factors in atherosclerosis, we identified matrilin-2, the collagen IV crosslinking enzyme peroxidasin as well as the poorly characterized MAM-domain containing 2 (Mamdc2) protein as being up-regulated in the ECM during atherogenesis. Intriguingly, three subunits of the osteoclast specific V-ATPase complex were strongly increased in mature plaques with an enrichment in macrophages thus implying an active de-mineralization function.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter Animal Models* ; Atherosclerosis ; Cardiovascular Function Or Biology ; Extracellular Matrix* ; Label-free Quantification ; Mechanism Of Action ; Mouse Models ; Stroke Biology, Biomarkers ; Subcellular Separation; Smooth-muscle-cells; Glomerular Extracellular-matrix; Coronary-artery-disease; Vascular Calcification; Deficient Mice; Gene Inactivation; Immune-system; Inflammation; Stroke; Identification
ISSN (print) / ISBN 1535-9476
e-ISSN 1535-9484
Quellenangaben Band: 17, Heft: 2, Seiten: 321-334 Artikelnummer: , Supplement: ,
Verlag American Society for Biochemistry and Molecular Biology
Verlagsort Bethesda
Begutachtungsstatus Peer reviewed