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. Author manuscript; available in PMC: 2022 Jun 18.
Published in final edited form as: Exp Eye Res. 2019 Jan 3;180:200–207. doi: 10.1016/j.exer.2019.01.001

Fig. 9. Decorin-mediated internalization of EGFR ensues via caveolar-mediated endocytosis.

Fig. 9.

Confocal photomicrograph showing inhibition of caveolae formation in hCSF cells using methyl-β-cyclodextrin (MβCD) that depletes cholesterol from the plasma membrane, rhDcn-induced internalization of EGFR was completely blocked (B) and EGFR was localized only in the plasma membrane (arrowheads). Contrary to this, rhEGF-induced internalization of EGFR was not affected (E, arrowheads) when treated with MβCD. When clathrin assembly was inhibited by chlorpromazine, a cationic amphiphilic drug that preferentially blocks the receptor recycling by preventing the adapter protein AP-2 of clathrin assembly on clathrin-coated pits, rhDcn-induced internalization of EGFR was observed (C, arrowheads) while rhEGF-induced internalization of EGFR was disrupted (F, arrowheads). The vehicle-treated (-dcn) showed no EGFR internalization as shown in Fig. 4A. Bar = 5 μM.