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. 2013 Sep 11;8(9):e74547. doi: 10.1371/journal.pone.0074547

Figure 5. Dephosphorylation of AMPK substrate i.e. acetyl CoA carboxylase (ACC) initiates neuritogenic effect of SIM.

Figure 5

A) Immunoblot showing SIM induced change in phosphorylation of ACC over a period of 2 hrs, 6 hrs and 12 hrs. SIM led to a significant (p < 0.05*) increase in pACC (Ser-79) levels at 2 hrs which was followed by a gradual decrease. Total ACC levels showed no change during SIM treatment. Error bar graph shows fold change (normalized to control) in pACC (Ser-79) levels at different time points (mean ± SEM; n = 4). B) Immunoblot showing modulation of ACC phosphorylation by SIM follows AMPK pathway. As evident, addition of AICAR (an AMPK activator) increased the phosphorylation of ACC either alone or in presence of SIM till 12 hrs. C) Morphology of SH-SY5Y cells under light microscope showing significant (p < 0.001) inhibition of SIM induced neuritogenesis in presence of acetyl CoA carboxylase (ACC) inhibitor i.e. 10 µM TOFA and fatty acid synthase (FAS) inhibitor i.e. 10 µM Cerulenin (Cerul.). Error bar graph shows the comparative difference in neurite lengths SIM, TOFA, SIM + TOFA, Cerulenin and SIM + Cerulenin treated cells for a period of 12 hrs (mean ± SEM; N = 50 cells per condition from 3 separate cultures). Morphology of PC12 cells under light microscope in presence of NGF or NGF + TOFA for a period of 3 days. Scale Bar = 100 µm.