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Fig. 3 | Journal of Translational Medicine

Fig. 3

From: Ca2+ dysregulation in cardiac stromal cells sustains fibro-adipose remodeling in Arrhythmogenic Cardiomyopathy and can be modulated by flecainide

Fig. 3

ER-dependent Ca2+-release through IP3Rs is larger in ACM C-MSC. A Representative tracings of the intracellular Ca2+ release evoked by CPA (30 μM) in C-MSC from HC donors and ACM patients. B Peak amplitude of CPA -evoked ER Ca2+ mobilization in HC and ACM C-MSC (n = 314 cells HC vs. n = 351 ACM; Two-tailed Student’s t-tests). C Representative tracings of the intracellular Ca2+ release evoked by ATP (100 μM) in C-MSC from HC donors and ACM patients. D Peak amplitude of ATP-evoked ER Ca2+ mobilization in HC and ACM C-MSC (n = 158 cells HC vs. n = 196 ACM Two-tailed Student’s t-tests). Expression of ATP2A2 E and ITPR2 F in total RNA extracts of C-MSC from HC donors and ACM patients. GAPDH was used as a house-keeping gene and qRT-PCR data are presented as the genes threshold cycles (Ct) with respect to the housekeeping gene GAPDH (ΔCt) (n = 6 biological replicates; Two-tailed Student’s t-tests). G Representative images of WB analysis of proteins extracted from HC and ACM C-MSC cultured in GM, hybridized with anti-SERCA2 ATPase and anti-IP3R antibodies. Immunostaining of the housekeeping H3 or Tubulin are shown for normalization. Densitometric analysis of SERCA2 ATPase (n = 8 biological replicates; H) and IP3R (n = 8 biological replicates; I) levels, normalized on H3 and Tubulin respectively (Two-tailed Student’s t-tests). Data information: mean ± SEM. *P < 0.05, **P < 0.01 and ***P < 0.0001

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