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Image Search Results
Journal: The Journal of Clinical Investigation
Article Title: Extracellular matrix proteomics identifies molecular signature of symptomatic carotid plaques
doi: 10.1172/JCI86924
Figure Lengend Snippet: ( A ) Schematic for detecting differentially expressed ECM proteins that also showed differential secretion in lipid-loaded human vascular SMCs. ( B ) The proteomics analysis of the conditioned media (“secretome”) showed the LGALS3BP level to be significantly higher in the lipid-loaded versus control SMCs ( n = 6, *** P = 0.005, paired t test). The box plot is as follows: black line, median; box edges, 1st and 3rd quartile; whiskers, furthest point within 1.5 times the interquartile range. ( C ) Immunofluorescence staining for LGALS3BP (red) in early atherosclerosis (human ascending aorta). Autofluorescence of elastin fibers (green). Scale bars: 200 μm. ( D ) Validation by immunoblotting. Note the co-detection of MMP9, FN1, LGALS3BP, and TNC upon lipid loading. SMCs from two different donors. Gelatin zymography for MMP2 was used as loading control. ( E ) Human aortic explants were either incubated with 50 pM MMP9 or left untreated for 24 hours. The degradation of FN1, TNC, and LGALS3B was examined by immunoblotting. MMP9 induces degradation of FN1 and TNC but releases LGALS3BP from human aortic explants. Aortic explants were from 2 different donors. Arrows indicate fragmentation products.
Article Snippet: In the Bruneck year 2000 evaluation and the SAPHIR study, the following proteins were measured by ELISA in plasma samples according to the manufacturers’ instructions: MMP9 from R&D Systems (DMP900); CHI3L1 from R&D Systems (DC3L10);
Techniques: Control, Immunofluorescence, Staining, Biomarker Discovery, Western Blot, Zymography, Incubation
Journal: The Journal of Clinical Investigation
Article Title: Extracellular matrix proteomics identifies molecular signature of symptomatic carotid plaques
doi: 10.1172/JCI86924
Figure Lengend Snippet: ( A ) Immunohistochemistry staining for LGALS3BP, S100A8/A9, CHI3L1, and MMP9 plus SMC (SMA, CNN1) and macrophage (CD68) markers. Scale bars: 500 μm. ( B ) Association between the biomarker candidates and atherosclerosis ( n = 560) and CVD ( n = 685) in the Bruneck study. Direction and strength of associations are coded by color and significance levels by size of frames. ORs are derived from logistic regression analysis, and hazard ratios from Cox models. ORs and hazard ratios are expressed for a 1-SD higher log e -transformed level of the given marker. Full details are presented in . Model 1 (M1) was adjusted for age (years) and sex. M2 was additionally controlled for standard vascular risk factors, including LDL cholesterol (mg/dl), HDL cholesterol (mg/dl), high-sensitivity CRP (mg/l), diabetes mellitus (0 vs. 1), hypertension (0 vs. 1), smoking (pack-years), and body mass index (kg/m 2 ). *Additionally adjusted for atherosclerosis score (mm).
Article Snippet: In the Bruneck year 2000 evaluation and the SAPHIR study, the following proteins were measured by ELISA in plasma samples according to the manufacturers’ instructions: MMP9 from R&D Systems (DMP900); CHI3L1 from R&D Systems (DC3L10);
Techniques: Immunohistochemistry, Staining, Biomarker Discovery, Derivative Assay, Transformation Assay, Marker