Fig. 5

The plasma HDL from ARDS patients promotes the dysfunction of primary pulmonary microvascular endothelial cells. Mouse lung microvascular endothelial cells (MLECs) were treated with N-HDL, A-HDL and PBS with human albumins as control (50 μg/ml, 24 h). Western blot analysis for junctional protein (VE-cadherin), vascular adhesion markers (VCAM1 and ICAM1) and Phospho-NF-κB p65. (n = 4 per group). b The monolayers of MLECs on transwell inserts were treated with HDLs (50 μg/ml, 24 h) and the permeability was determined by the diffusion of tracer (FITC-dextran) into the lower compartment. The permeability change was presented as the fold change of fluorescence intensity relative to controls (n = 4 per group). c qPCR analyses of the mRNA expressions of cytokines (TNF-a and IL-6) in MLECs treated with HDLs (50 μg/ml, 12 h). (n = 5 per group). *p < 0.05 and **p < 0.01 versus control group; ^&p < 0.05 and ^&&&p < 0.001 versus N-HDL treatment group. VCAM1 vascular cell adhesion molecule-1, ICAM1 intercellular adhesion molecules-1, Ctl control, N-HDL HDL from normal subjects, A-HDL HDL from ARDS patients