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. 2022 May 25;29(11):2316–2331. doi: 10.1038/s41418-022-01018-8

Fig. 6. Enhanced lipid hydrolysis is responsible for phospholipid remodeling and mitochondrial defects in Plin2-/- mESCs.

Fig. 6

a CL, PE, and PC contents in mitochondria of WT and Plin2-/- mESCs (KO1 and KO2) treated with DMSO or ATGLi (10 μM Atglistatin). Data are mean ± SD, n = 3 biological replicates. Two-tailed unpaired t-tests. ***P < 0.001, **P < 0.005. b Representative TEM images of mitochondria and quantification of mitochondria with disorganized cristae in WT and Plin2-/- mESCs (KO1 and KO2) treated with DMSO or ATGLi (10 μM Atglistatin). Scale bar, 1 μm. Data are mean ± SD, n = 3 biological replicates (each >100 mitochondria). Two-tailed unpaired t-tests. **P < 0.005. c Maximal mitochondrial respiration in WT and Plin2-/- mESCs (KO1 and KO2) treated with DMSO or ATGLi (10 μM Atglistatin). Data are mean ± SEM, n = 3 biological replicates. Two-tailed unpaired t-tests. ***P < 0.001. d Acetyl-CoA content in WT and Plin2-/- mESCs (KO1 and KO2) treated with DMSO or ATGLi (10 μM Atglistatin). Data are mean ± SD, n = 3 biological replicates. Two-tailed unpaired t-tests. *P < 0.05. e Western blot analysis and quantification of H3K27ac levels in WT and Plin2-/- mESCs (KO1 and KO2) treated with DMSO or ATGLi (10 μM Atglistatin) on day 3 of differentiation. Data are mean ± SD, n = 3 biological replicates. Two-tailed unpaired t-tests. ***P < 0.001.