Fig. 8

ALPL deficiency promoted the internalization of L-type Ca²⁺ channels in HPP patient-derived BMSCs. a The expression of ALPL on the membrane and cytoplasm was decreased in BMSCs from two HPP patients compared with that of normal human BMSCs. β-actin was used as a protein loading control. b Intracellular Ca²⁺ imaging analysis showed that KCl-induced Ca²⁺ influx was significantly decreased in cultured BMSCs from HPP patients compared with that of normal human BMSCs. c Overexpression of ALPL or transfection with DN-Dyn1 in BMSCs from A1 patients showed elevated KCl-induced Ca²⁺ influx. d Overexpression of ALPL or transfection with DN-Dyn1 in BMSCs from A2 patients showed elevated KCl-induced Ca²⁺ influx. e Representative images of confocal laser scanning microscopy showing the membrane location of Ca_V1.2 and Ca_V1.3 in control BMSCs, A1 BMSCs, A2 BMSCs, A1 and A2 BMSCs overexpressing ALPL, and A1 and A2 BMSCs transfected with DN-Dyn1. Scale bar, 10 μm. The representative results from three independent experiments are shown. Error bars represent the s.d. from the mean values. *P < 0.05; **P < 0.01