Fig. 6: Knockdown of NMDAR subunits NMDAζ1, NMDAε2, and NMDAε4 promoted apoptosis, intracellular Ca2+ influx, ROS production, and restrained mitochondrial O2 consumption rate. | Cell Death Discovery

Fig. 6: Knockdown of NMDAR subunits NMDAζ1, NMDAε2, and NMDAε4 promoted apoptosis, intracellular Ca2+ influx, ROS production, and restrained mitochondrial O2 consumption rate.

From: NMDARs antagonist MK801 suppresses LPS-induced apoptosis and mitochondrial dysfunction by regulating subunits of NMDARs via the CaM/CaMKII/ERK pathway

Fig. 6

A Representative flow cytometry images and analysis of cell apoptosis with live cells (B), death (C), early apoptosis (D), and late apoptosis in HUVECs transfected with control siRNA, NMDAζ1 siRNA, NMDAε1 siRNA, NMDAε2 siRNA, NMDAε3 siRNA, or NMDAε4 siRNA. F Flow cytometry graphs and G analysis of Ca2+ influx in HUVECs transfected with control siRNA, NMDAζ1 siRNA, NMDAε1 siRNA, NMDAε2 siRNA, NMDAε3 siRNA, or NMDAε4 siRNA. H Flow cytometry graphs and I analysis of ROS in HUVECs transfected with control siRNA, NMDAζ1, NMDAε1 siRNA, NMDAε2 siRNA, NMDAε3 siRNA, or NMDAε4 siRNA. J Seahorse XF24 Extracellular Flux Analyzer detected mitochondrial O2 consumption rate, K basal respiration rate, L maximal respiration rate, and M ATP production in HUVECs after transfection with different siRNA. (Data are presented as mean ± SEM, ***P < 0.001, **P < 0.01, *P < 0.05 vs. control siRNA).

Back to article page