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. Author manuscript; available in PMC: 2018 Apr 19.
Published in final edited form as: Handb Exp Pharmacol. 2018;245:271–312. doi: 10.1007/164_2017_62

Figure 5. Fluid phase uptake of hA monomers and oligomers by pancreatic cells.

Figure 5

(A) Initial entry (1h) of hA monomers (top panel) and oligomers (bottom panel) is through dynamin-independent macropinocytosis in RINm5F cells. Cells were treated with various endocytotic inhibitors EIPA, CytD, Wort or Dyn for 1 hour followed by hA (green) (10 μM) for an additional 1 hour at 37°C. Dextran (red) at 40μg/ml was finally added for 30 minutes. Confocal microscopy revealed a significant reduction in internalization and an increase in PM accumulation of hA monomers (green) and dextran (red) in the presence EIPA, CytD or Wort but not Dyn when compared to controls. (A, top panel and graph). Similar internalization pathway was also demonstrated for hA oligomers and dextran within the first hour (A, bottom panel and graph). (B) Late entry (24h) of hA oligomers but not monomers is through dynamin-independent macropinocytosis in RINm5F cells. Note no significant change in the cellular distributions of hA monomers (top panel, graph) in the presence of EIPA, CytD, Wort or DN dyn1K44A when compared to controls. On the contrary, dextran internalization was completely blocked with these macropinocytotic inhibitors but not with DN dyn1K44A (A, top panel and graph). Marked inhibition in internalization of hA oligomers and dextran was observed following treatments with EIPA, CytD or Wort but not with DN dyn1K44A (A, bottom panel and graph). Bar 10μm. **p<0.01, hA vs. hA plus inhibitors, ##p<0.01, dextran vs. dextran plus inhibitors, NS p>0.05, n=9. Significance established by ANOVA followed by Dunnett-Square test.