Oxidative Medicine and Cellular Longevity / 2020 / Article / Fig 5

Research Article

Drp-1 as Potential Therapeutic Target for Lipopolysaccharide-Induced Vascular Hyperpermeability

Figure 5

Inhibition of Drp-1 blocked mitophagy and exacerbated LPS-induced vascular hyperpermeability. Mice were subjected to LPS (5 mg/kg) and treated with either mdivi-1 (3 mg/kg) or vehicle for 60 min. (a) Western blotting was used to assess mitophagy-related proteins. (b) TOMM20 level quantification; (c) TIMM23 level quantification; (d) TFAM level quantification; (e) PGC-1α level quantification. (f) PINK1 level quantification; (g) cytoplasmic Parkin level quantification; (h) mitochondrial Parkin level quantification. (i) Intravital microscopy analysis (100x magnification) of mesenteric postcapillary venules with altered permeability (100x magnification). Scale bars, 50 μm. (j) Quantification of vascular permeability. The represent the data ( in each group). An asterisk () indicates vs. various groups. Drp-1: Dynamin-related protein-1; LPS: lipopolysaccharide; TOMM20: translocase of outer mitochondrial membrane 20; TIMM23: translocase of inner mitochondrial membrane 23; PGC-1α: PPARG coactivator 1 alpha; TFAM: transcription factor A mitochondria; PINK1: tensin homolog (PTEN)-induced putative kinase 1; Cyto.: cytoplasmic; Mito.: mitochondrial; COX IV: cytochrome C oxidase subunit 4.

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