Fig. 2From: c-Jun-mediated miR-19b expression induces endothelial barrier dysfunction in an in vitro model of hemorrhagic shockc-Jun silencing attenuates H/R-induced increases in pri-miR-19b, mature miR-19b, and cell surface syndecan-1. A c-Jun expression in cells transfected with c-Jun siRNA (si) or scrambled RNA (sc) then exposed to normoxia (Norm) or H/R. B The levels of pri-miR-19b were measured by RT-qPCR in the cells. C The levels of miR-19b were measured by RT-qPCR in the cells. Mean ± SE for four experiments. D Representative phase contrast images. E Cells were immunostained with anti-syndecan-1 antibody and images captured. F The fluorescence intensity results were presented as mean ± SE for four experiments. G and H Inhibition of either miR-19b by oligo inhibitors (19b-in) or c-Jun by siRNA (si) attenuated H/R-induced monolayer hyperpermeability. Shown were the measurements of monolayer permeability detected by FITC-dextran. Mean ± SE for four experimentsBack to article page