Fig. 6
From: Targeting NLRP3 signaling reduces myocarditis-induced arrhythmogenesis and cardiac remodeling
Effects of the NLRP3/CaMKII axis on Ca2+ regulatory proteins in rat RVOTs. Representative Western blots and summary data for sarcoplasmic/endoplasmic reticulum Ca2+ ATPase 2a, CaMKII phosphorylated at Thr286, RyR2, total phospholamban, RYR phosphorylated at Ser2808, phospholamban phosphorylated at Thr17, protein kinase A, Cav1.2, NLRP3, nuclear factor-κB, and interleukin-1β expression in the RVOT tissues of the control (healthy rats; n = 7), experimental (rats with myocarditis; n = 7), and treatment (MCC950-treated rats with myocarditis; n = 7) groups. Glyceraldehyde-3-phosphate dehydrogenase served as a loading control. CaMKII, Ca2 + /calmodulin-dependent protein kinase II; RYR, ryanodine receptor; RVOT, right ventricle outflow tract