Skip to main content
. 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 3. High affinity AM-R-dependent and low affinity AM-R-independent hA transport operate in pancreatic cells.

Figure 3

Rin-m5F (A) and human islet cells (B) were incubated with 100 nM or 10 μM hA either in the presence or absence of the AM-R antagonist, AC-187 (1–100 nM) for 24 hours. hA accumulation on the cell PM and subsequent internalization was concurrently assessed with quantitative confocal microscopy analysis. (A) Confocal microscopy analysis of hA uptake in Rin-m5F cells is shown. When low concentration of hA (100 nM) was used, hA monomer internalization was significantly inhibited with increasing concentrations of AC-187 (top panel, graph). A corresponding increase in hA accumulation on cell PM was observed. In contrast to this high affinity uptake process, hA monomer/oligomer uptake at high (10 μM) was not affected with increasing concentrations of AC-187 (bottom panel, graph). (B) Confocal microscopy analysis of hA uptake in cultured human islet cells is depicted. Note a dose-dependent inhibition of hA uptake by AC-187 at lower (100 nM) but not higher (10 μM) hA concentrations, revealing high- and low-affinity hA transport mechanism in β-cells, respectively. Significance established at p<0.05 by ANOVA followed by Dunnett-Square test. Bar 5μm.