Fig. 4: Knockdown of CHCHD2 increases cellular ROS and apoptosis, and deceases cell viability. | Cell Death & Disease

Fig. 4: Knockdown of CHCHD2 increases cellular ROS and apoptosis, and deceases cell viability.

From: CHCHD2 up-regulation in Huntington disease mediates a compensatory protective response against oxidative stress

Fig. 4

A qRT-PCR results shown that knockdown of endogenous CHCHD2 by lentiviral shRNA reduced the expression of this gene in Q7 and Q111 cells. n = 3 independent biological replicates. B Cellular ROS was determined by H2DCFDA, and the corresponding mean fluorescence intensity (MFI) with values were shown in the upper histogram and plotted in the graph below. n = 3 biological replicates. C The cell viability was determined by CellTiter-Glo assay, and the relative cell viability to untreated Q7 shControl group was plotted in the graph. n = 7 biological replicates. D Cleaved Caspase-3 expression levels in Q7 and Q111 cells knockdown by shControl and shCHCHD2 was determined by immunoblotting. n = 3 independent biological replicates; Values shown as mean ± SEM; *p < 0.05, **p < 0.01, and ****p < 0.0001 for shown comparisons, and #p < 0.05, ####p < 0.001, and #####p < 0.0001 relative to the corresponding Q7 group was determined by two-way ANOVA analysis followed by a Bonferroni post hoc multiple-comparison test.

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