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Fig. 4 | Molecular Neurodegeneration

Fig. 4

From: High-density lipoproteins suppress Aβ-induced PBMC adhesion to human endothelial cells in bioengineered vessels and in monoculture

Fig. 4

HDL suppression of Aβ-induced inflammation is independent of eNOS and S1P. a Intracellular NO production was measured by treating hCMEC/D3 with 100 μg/mL HDL in the presence of 1 μM DAF-2 for 6 h. Fluorescence was measured at 485 nm. b Phosphorylation of eNOS was measured by treating hCMEC/D3 with 100 μg/mL HDL for 15 min before immunoblotting for phosphorylated eNOS (p-eNOS) or total eNOS. Representative immunoblots are shown in (c). hCMEC/D3 were pretreated for 1 h with the eNOS inhibitor L-NAME (d-f) or the S1P1 and S1P3 inhibitor VPC23019 (g-i) followed by 100 μg/mL HDL for 2 h. Cells were then stimulated with 0.1 μM Aβ40 (d,g) Aβ42 monomers, (e,h) or 1 ng/mL of TNF-α (f,i) for 3 h before testing PBMC adherence. Graphs represent means ± SD of adhered PBMC relative to vehicle treated cells for at least 5 independent trials. *p < 0.05, **p < 0.01, ***p < 0.001 * p < 0.05, **p < 0.01, ***p < 0.001 versus vehicle, § p < 0.05, §§ p < 0.01, §§§p < 0.001 versus Aβ or TNF-α

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