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. 2016 Dec 22;6:39513. doi: 10.1038/srep39513

Figure 3. Ang II enhances the interaction of nephrin with β-arrestin2 through AT1 receptor activation.

Figure 3

(a) HEK293T cells expressing nephrin, β-arrestin2 and the AT1-receptor were stimulated with Ang II. Ang II stimulation enhances the binding of β-arrestin2 to nephrin in a time dependent fashion. The maximum enhancement of 3-fold is seen after 60 min of Ang II stimulation (**Kruskal-Wallis test n = 12, p = 0.026). (b) HEK293T cells lacking the AT1 receptor do not show enhanced binding of nephrin to β-arrestin2 under stimulation with Ang II (**n = 9, p = 0.0019). The Ang II mediated enhanced binding of β-arrestin2 to nephrin is blocked by the AT1 receptor antagonist (c) Candesartan [100 nM] (*n  =  3, p = 0.03, ns = 0.314). Comparable amounts of nephrin fusion protein expression and its control were controlled by western blot (experiments were conducted in HEK293T cells). The expression of the transfected nephrin fusion proteins and its control is shown in the supplemental Fig. 1Sb–d. The Ang II mediated activation of ERK is shown in the supplemental Fig. 3Sa.