Endothelial Cell Inflammation and Barriers Are Regulated by the Rab26-Mediated Balance between β2-AR and TLR4 in Pulmonary Microvessel Endothelial Cells

Figure 1

Rab26 regulates LPS-induced inflammation and hyperpermeability in HPMECs. Mock: vector; Rab26^WT: Rab26 wild type; Rab26^QL: Rab26 Q123L; Rab26^NI: Rab26 N177I. (a) Confocal microscopy analyses of the Rab26 protein expression profiles. HPMECs were transfected with HA-tagged Rab26 plasmids for 72 h and treated with LPS (1 μg/mL) for 6 h. Then, the cells were incubated with the Rab26 (1 : 200 dilution) antibody followed by labeling with Alexa Fluor 594-conjugated secondary antibody (1 : 300 dilution). Red: Rab26; blue: cell nuclei. Scale bars: 25 μm. (b) Western blots showed the Rab26 expression after transfection with the HA-tagged Rab26 plasmids and LPS treatment. The histograms show the quantitative analysis of the protein expression levels which were normalized to GAPDH expression. (c, d) Expression of inflammatory factors after transfection with the Rab26 plasmids by ELISA (IL-6, IL-17A, IL-8, and TNF-α). (e) BSA permeability analysis of the HPMECs transfected with the DsRed-tagged Rab26 plasmids and treated with LPS. The data are the (). versus the control group; ^{^} versus the mock group.

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