Fig. 4: VDAC1 knockdown impairs intracellular calcium buffering capacity.
From: Ischemic postconditioning confers cerebroprotection by stabilizing VDACs after brain ischemia
a Immunoblots and quantification of VDACs in VDAC1+/+ and VDAC1+/− HT22 cells. Relative levels were normalized to VDAC1+/+ groups (n = 3). Actin was used as a loading control. Data are the mean ± SD of three independent experiments. *P < 0.05; n.s., not significant; unpaired t-test. b Resting cytosolic Ca2+ levels ([Ca2+]i) in HT22 cells detected by Fura-2/AM. Data are the mean ± SD (n = 39). n.s., not significant; unpaired t-test. c Time-lapse image of representative calcium fluorescence induced by ionomycin (2 μM) treatment in VDAC1+/+ or VDAC1+/− HT22 cells transfected with GCaMP6f plasmid. Scale bar, 50 μm. d [Ca2+]i fluctuations induced by ionomycin (2 μM) treatment in VDAC1+/+ or VDAC1+/− HT22 cells detected by Fura-2/AM. Data represent the mean ± SEM (n = 40 for VDAC1+/+ HT22 cells; n = 50 for VDAC1+/− HT22 cells). ***P < 0.01 (10–18 min after ionomycin treatment); Two-way ANOVA. e Mitochondrial [Ca2+] fluctuations in VDAC1+/+ or VDAC1+/− HT22 cells detected by Rhod-2/AM under the stimulation of calcium (2 μM). Data represent the mean ± SEM (n = 43 for VDAC1+/+ HT22 cells; n = 35 for VDAC1+/− HT22 cells). Two-way ANOVA
