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. 2021 Dec 18;79(1):57. doi: 10.1007/s00018-021-04065-5

Fig. 1.

Fig. 1

(A) Time-course of SRF activation by angiotensin II (1 nmol/l AII) in HEK293 cells transfected with AT1R. N = 24. (B) AII-induced SRF activity in responsive cells (= analogue response). (C) AII-induced percentage SRF-positive cells of transfected cells (= digital response). (D) Concentration–response curve of SRF activation by AII after 24 h. N = 18. (E) Synergistic action of 10 µg/l EGF and AII on SRF activity (N = 18; t = 24 h). (F) Synergistic SRF activation in responsive cells (= analogue response). (G) Synergistic increase of the percentage of SRF-positive cells (= digital response). (H) Estimation of the maximum effect (Emax) elicited by AII in the absence and presence of EGF and of the half-maximum AII concentration (EC50) from the data in panel (E) and SF05 (mean ± SD). (I) AII-induced SRF activity in the absence and presence of 1 µg/l EGF (N = 18; t = 24 h). (J) AII-induced SRF activity in the absence and presence of 10 µg/l EGF (N = 18; t = 24 h). (K) AII-induced SRF activity in the absence and presence of 100 µg/l EGF (N = 18; t = 24 h). (L) The action of 1 nmol/l AII and the synergistic action of 1 nmol/l AII + 10 µg/l EGF are prevented by the AT1R blocker losartan (L, 1 µmol/l; N = 12, t = 24 h). *p < 0.05 versus control, if not indicated otherwise