Additional file 1 of Ca2+ dysregulation in cardiac stromal cells sustains fibro-adipose remodeling in Arrhythmogenic Cardiomyopathy and can be modulated by flecainide

Additional file 1: Text. IP3-induced intracellular Ca2+ release and SOCE drive spontaneous Ca2+ oscillations in ACM C-MSC. Fig. S1. Resting [Ca2+]iin C-MSC. Fig. S2. Suramin and MRS-2179 inhibit the spontaneous Ca2+ activity in ACM C-MSC. Fig. S3. CaMKII expression in human-derived C-MSC. Figure S4: SOCE and IP3Rs drive the spontaneous Ca2+ oscillations in ACM C-MSC. Fig. S5. Effect of XeC on spontaneous Ca2+ oscillations in ACM C-MSC. Fig. S6. Contribution of VOCC and reverse-mode NCX to spontaneous Ca2+ oscillations in ACM C-MSC. Fig. S7. IP3R, but not RYR, contribute to spontaneous Ca2+ oscillations in ACM C-MSC. Fig. S8. Ryanodine do not affect spontaneous Ca2+ oscillations in ACM C-MSC. Fig. S9. Voltage-Gated Ca2+ Entry is lower in ACM C-MSC. Fig. S10. Nifedipine inhibits Ca2+ response to High K+. Fig. S11. Blocking constitutive SOCE prevents ER Ca2+ release in ACM C-MSC. Fig. S12. Spontaneous Ca2+ oscillations during adipogenesis. Fig. S13. BAPTA inhibit the spontaneous Ca2+ activity of ACM C-MSC. Fig. S14. PLIN1 modulation in ACM C-MSC. Fig. S15. PKP2 silencing in C-MSC. Table S1. Clinical data of ACM patients enrolled for biopsy samples. Table S2. Clinical features of the deceased tissue donors (with healthy heart) enrolled in this study. Table S3. Primer sequences 5’ - 3’. Table S4. Primary antibodies