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. 2020 Oct 20;11:5303. doi: 10.1038/s41467-020-18947-y

Fig. 1. ht31 prevents glucose/NF546-induced cAMP in human cells.

Fig. 1

a Average ICUE3-PM FRET trace (mean = solid line; SEM = shade) in response to application of 10 μM ht31 and after 1 μM forskolin in human arterial myocytes. Time courses of the average ICUE3-PM FRET traces (mean = solid line; SEM = shade) in human arterial myocytes in response to b 15 mM D-glucose (D-glu) and c 500 nM NF546 and after 1 μM forskolin in control (CT) and ht31-treated cells. d Plot of maximum FRET responses for human male/female arterial myocytes exposed to the ht31 peptide alone (n = 17 cells/2 humans), 15 mM D-glu (n = 19 cells/3 humans for −ht31 and n = 36 cells/3 humans for +ht31) and NF546 (n = 18 cells/3 humans for −ht31 and n = 14 cells/3 humans for +ht31) in the absence and presence of forskolin. *P < 0.05 with Kruskal–Wallis one-way ANOVA with Dunn’s multiple comparisons. The single asterisks highlight significant differences between all datasets in the absence of forskolin. The double asterisks indicate a statistical difference within the same experimental group in the absence and presence forskolin. P = 0.0002 for 15 mM D-glu-ht31 and ht31-ht31 + 15 mM D-glu + forskolin. P = 0.0002 for NF546-NF546 + forskolin. All other significant P values are <0.0001. Data represent mean ± SEM. Source data are provided as Source data file.