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. 2020 Nov 25;70(2):562–576. doi: 10.2337/db20-0660

Figure 1.

Figure 1

EGFR activation increased rubicon expression and inhibited autophagic flux in cultured podocytes. A: Exposure of podocytes to high glucose (HG) led to activation of EGFR signaling, and increases in SQSTM1 and rubicon expression were inhibited with AG1478, an EGFR tyrosine kinase inhibitor. B: High glucose–induced beclin-1 inhibition and rubicon stimulation were inhibited with AG1478 (C). AG1478 inhibited HG-induced phosphorylated (p-)S6K and phosphorylated S6 activation. D and E: AG1478 increased LC3B abundance (N = 10 fields per group) and LC3B autophagosomes in podocytes. For measurement of LC3B II turnover, the podocytes were examined without (−) or with (+) treatment with 50 μmol/L chloroquine (CQ.) for 16 h. *P < 0.05 and **P < 0.01 vs. high glucose group, N = 3 independent repeats, one-way ANOVA with Bonferroni post hoc test. AU, arbitrary units; Veh, vehicle.