Skip to main content
. 2025 Feb 7;292(9):2359–2380. doi: 10.1111/febs.70006

Fig. 4.

Fig. 4

Pharmacological activation of AMPK restores MMP in mtDNA‐depleted cells. (A) Immunoblotting indicates levels of phosphorylated AMPK (p‐AMPK) and total AMPK in uninduced cells and in cells expressing PolɣD1135A (4‐days induction) prior (−) and following AMPK activation with 100 μm A‐769662 for 48 or 72 h. A representative image of n = 4–5 is shown. GAPDH is provided as loading control. (B) Quantification of p‐AMPK/AMPK ratios from A. n = 4–5. (C) MMP in uninduced (gray) cells and cells expressing PolɣD1135A (pink; 4‐days induction) prior (−) and following AMPK activation with 100 μm A‐769662 for 48 or 72 h; n = 3. (D) Immunoblotting indicates levels of phosphorylated AMPK (p‐AMPK) and total AMPK in uninduced cells and in ones expressing PolGD1135A following silencing of AMPK using siRNA against α1/α2 AMPK, or a scrambled siRNA as negative control. A representative image of n = 3 is shown. (E) MMP in uninduced (gray) cells and cells expressing PolɣD1135A (pink; 4‐days induction) following AMPK silencing (striped bars) and/or A‐769662 treatment (darker shade) from the experiment in D; n = 3. (F) Cell proliferation assessed by cell number after a 96‐h treatment with 100 μm A‐769662 (pink) in uninduced cells or ones induced to express PolɣD1135A for 6 days; n = 2. Results were analyzed by unpaired t test; error bars in the graphs represent standard deviation. (n, number of biological replicates; ns, not significant; *P ≤ 0.05; **P ≤ 0.01; ***P ≤ 0.001; ****P ≤ 0.0001).