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. Author manuscript; available in PMC: 2018 Nov 1.
Published in final edited form as: J Mol Cell Cardiol. 2017 Sep 18;112:95–103. doi: 10.1016/j.yjmcc.2017.09.006

Fig. 3. All three IP3R isoforms contribute to hypertrophic signaling by ET-1.

Fig. 3

(A) Neonatal cardiomyocytes were transfected with control or IP 3R siRNA as indicated. Cells were treated with ET-1 and oscillation frequency was quantified from at least 4 separate experiments (control n=6, 1 n=6, 2 n=7, 3 n=6, 1/2 n=6, 2/3 n=5, 1/3 n=5 and 1/2/3 n=4). (B). Western blot of indicated proteins after 48 hours or 6 days treatment with 100 nM ET-1. (C). Quantification of IP 3R levels after ET-1 treatment for 48 hours or 6 days expressed as percent of control. (D) Atrial natriuretic peptide (ANP) levels after 48 hours and 6 days treatment with ET-1. Blotting with alpha-fodrin was used as control. (E) NFAT activity using luciferase reporter construct after ET-1 treatment for the indicated times in control siRNA and triple IP3R siRNA transfected cardiomyocytes. (F) Average cell area before and after 48 hours treatment with ET-1. Neonatal cardiomyocytes were transfected with control siRNA and triple IP 3R siRNA. All data are shown as mean ± SEM, *P < 0.01 vs control.