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Fig. 4 | Arthritis Research & Therapy

Fig. 4

From: Endothelial activation and injury by microparticles in patients with systemic lupus erythematosus and rheumatoid arthritis

Fig. 4

Microparticles (MPs) and microparticles that form immune complexes (MPs-ICs) from patients with systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) induced intercellular spaces (GAPs) formation, actin depolymerization, and increased expression of VE-cadherin in cytosol. a Representative images of the fluorescent labeling of the nucleus (blue), F-actin (actin filaments, in green), VE-cadherin (red), and the superposition of these images (merge) for human umbilical vein endothelial cells (HUVEC) without treatment (vehicle), and treated with MPs or MPs-ICs from patients with RA and SLE for 24 h. Large arrows indicate the presence of GAPs, small arrows indicate actin beads, and arrowheads indicate nuclear condensation and fragmentation; ×20 objective. b Fluorescence profile for each label shown in a. White arrows indicate the points from which the line was drawn (region of interest (ROI)) to determine the fluorescence profile, and black arrows indicate the plasma membrane of the cells; ×60 objective. c GAPs area and perimeter quantification after treatment with MPs and MPs-ICs from patients with RA and SLE. All of the GAPs found in at least 5 fields were measured for each treatment by using a ×20 objective. Data are presented as the median ± interquartile range. Kruskal–Wallis, *p ≤ 0.05, **p < 0.01, ***p < 0.001, n = 3

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