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. 2009 Oct 15;59(1):190–199. doi: 10.2337/db09-0655

FIG. 7.

FIG. 7.

Nephrin trafficking depends on actin and is essential for GSIR. A: GFP-nephrin–transfected into MIN6 cells is mainly localized at the sites of cell-to-cell contact in 2 mmol/l glucose. Upon glucose stimulation, nephrin undergoes a time-dependent endocytosis. B: Actin stabilization with 0.5 μmol/l jasplakinolide prevented glucose-induced relocation of GFP-nephrin from the plasma membrane to the cytoplasm. C: Actin depolymerization with cytochalasin D led instead to nephrin redistribution from plasma membrane to the cytoplasm in a dose-dependent manner. D: The positive effect of nephrin overexpression on GSIR was also totally prevented by pretreatment with 0.5 μmol/l jasplakinolide. *P < 0.05, **P < 0.01. All experiments were repeated four times. E: MIN6 cells exposed to cytochalasin D (Cy D), jasplakinolide (Jasp), and phalloidin were analyzed for the change in F-actin content compared to control untreated cells. While an increased G-to-F actin ratio was observed with CyD (***P < 0.001), both jasplakinolide and phalloidin treatment resulted in a 50% reduction of G-to-F actin ratios (*P < 0.05). (A high-quality color digital representation of this figure is available in the online issue.)