Drp-1 as Potential Therapeutic Target for Lipopolysaccharide-Induced Vascular Hyperpermeability
Depletion of Drp-1 aggravates LPS-induced activation of mitochondria-dependent apoptosis and endothelial barrier disruption. PMVECs were transfected with Drp-1 siRNA (a scrambled siRNA was used as the control) and exposed to LPS (500 ng/ml) for 24 h. (a) Fluorescent inverted microscopy (200x magnification) determination of JC-1 intracellular green and red fluorescence. Scale bars, 50 μm. (b) JC-1 emitted intracellular green and red fluorescence quantification. (c) Luciferase-based assay for intracellular ATP levels. (d) Western blotting assessment of cleaved caspase-3 and cleaved caspase-9 levels. (e) Densitometry to quantify cleaved caspase-3 levels. (f) Densitometry to quantify cleaved caspase-9 levels. (g) FITC-dextran assessment of the permeability of an endothelial cell monolayer. The represent the data ( in each group). An asterisk () indicates vs. the various groups. Drp-1: Dynamin-related protein-1; LPS: lipopolysaccharide; FITC: fluorescein isothiocyanate.
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