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. Author manuscript; available in PMC: 2023 Jul 21.
Published in final edited form as: Nat Cardiovasc Res. 2022 Dec 12;1(12):1174–1186. doi: 10.1038/s44161-022-00175-w

Fig. 4 |. ANGPT1 release from platelets is influenced by sGC via the PKC pathway.

Fig. 4 |

a, ANGPT1 release by WT platelets incubated with 150 ppm BAY-747 or vehicle (n = 4 sample pairs from independent animals). b, WT neutrophil adhesion to WT ECs after incubation with supernatant from n = 7 activated WT platelets from independent animals that were preincubated with either vehicle or 150 ppm BAY-747. c, Inhibition of IP3-R (10 μM 2-APB), PKC (5 μM Ro 32–0432), PKG (10 μM KT-5823) and measurement of ANGPT1 release from platelets (n = 6). One outlier was removed from the PKG group (n = 5) according to the ROUT test. d, Inhibition of mitogen-activated protein kinase (MAPK) (10 μM VX-702), cyclin-dependent kinase (CDK) 2/5/9 (100 nM dinaciclib), extracellular signalregulated kinase (ERK) (10 μM ravoxertinib), and Akt kinase (1 μM MK-2206) and measurement of ANGPT1 release from platelets (n = 6). Each symbol represents paired samples derived from independent animals. a,b, Two-sided paired t-test. c,d, Mixed-effects analysis (ANOVA with Dunnett multiple comparison test). Data are the mean ± s.e.m.