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. 2021 Sep 8;46:102127. doi: 10.1016/j.redox.2021.102127

Fig. 3.

Fig. 3

PEMT deficiency increases mitochondrial CoQ content in mammalian cells and tissues. (A) Effect of inhibiting PEMT activity in PEMT-expressing McArdle 7777 hepatoma cells by 3-deazaadenosine (DZA) on mitochondrial CoQ9 content (n = 4). (B) Hepatic mitochondrial CoQ9 content in Pemt+/+ and Pemt–/– mice fed chow (n = 6). (C) Hepatic mitochondrial CoQ9 content in Pemt+/+ and Pemt–/– mice fed HFD for 6 weeks (n = 6–8). (D) Mitochondrial CoQ9 content in mice treated with adeno-associated virus (AAV) expressing Pemt or GFP control (n = 3–6). (E) Effect of anti-sense oligonucleotide (ASO) mediated knockdown of PEMT in differentiated 3T3-L1 adipocytes on PEMT gene expression as determined by qPCR (n = 4). (F) Mitochondrial CoQ9 content in differentiated 3T3-L1 adipocytes treated with either control or anti-PEMT ASO (n = 4). (G) White adipose tissue mitochondrial CoQ9 content in Pemt+/+ and Pemt–/– mice fed HFD for 6 weeks (n = 6–8) (H) Mitochondrial SAM/SAH ratio in mice treated with adeno-associated virus (AAV) expressing Pemt or GFP control (n = 3–6). Data and error bars depict mean ± s.e.m. *P ≤ 0.05 and ns indicates ‘not significant’ as determined by Mann-Whitney (A-C, E-G) or Kruskal-Wallis test (D, H).