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. 2021 Sep 1;8:724846. doi: 10.3389/fcvm.2021.724846

Figure 4.

Figure 4

FARS2 silencing causes mitochondrial dysfunction in human umbilical vein endothelial cells (HUVECs). (A) The oxygen consumption rate (OCR) in HUVECs transfected with siCtrl or si-FARS2. The HUVECs were seeded 48 h after transfection with siRNAs and 12 h before analysis using a Seahorse XF24 analyzer. The OCR was measured continuously throughout the experimental period, both at baseline and in the presence of the indicated drugs. (B) Non-mitochondrial respiration, basal respiration, maximal respiration, proton leak, ATP production, and spare respiratory capacity in control and FARS2-deficient HUVECs. The measurements were made in triplicate (mean and SEM). **P < 0.01, ***P < 0.001, ****P < 0.0001. (C) The effects of FARS2 knock-down on intracellular reactive oxygen species production by HUVECs. The measurements were made in triplicate (mean and SEM). *P < 0.05, (D) Quantification of total ATP levels in HUVECs 48 h after transfection with the indicated siRNAs. The measurements were made in triplicate (mean and SEM). **P < 0.01.