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Fig. 4 | Diabetology & Metabolic Syndrome

Fig. 4

From: Activation of mTOR mediates hyperglycemia-induced renal glomerular endothelial hyperpermeability via the RhoA/ROCK/pMLC signaling pathway

Fig. 4

HG induced the formation of stress fibers and intercellular gaps in a RhoA/ROCK pathway–dependent manner. a HRGECs were incubated with 5.5 mM glucose (NG) or 30 mM glucose (HG) and/or the ROCK inhibitor Y-27632 (10 μM) for 24 h. F-actin stress fiber formation was assessed using FITC-phalloidin staining. Cells were stained for F-actin (green) and DAPI (blue) and then imaged. b The intercellular gap area in each group (n = 3). c Western blot analysis of MLC phosphorylation. de Preincubation with Y-27632 (10 μM) significantly reduced the HG-induced increase in permeability according to TEER measurements and the HRP-albumin leakage assay (n = 3). HG, high glucose; HRGECs, human renal glomerular endothelial cells; NG, normal glucose; MLC, myosin light chain; TEER, transendothelial electrical resistance; HRP, horseradish peroxidase. * indicates p < 0.05 vs. the NG group. # indicates p < 0.05 vs. the HG group

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