Fig. 5.
Exposure of human embryonic stem cell–derived neurons to propofol altered the expression of the mitochondrial fission-related protein and did not affect mitochondrial fusion. (A) Western blotting was used to assess the expression of dynamin-related protein 1 (Drp1), a protein responsible for inducing mitochondrial fission. Drp1 becomes activated when phosphorylated at the Ser616 position. Exposure of human embryonic stem cell–derived neurons to 6 h of 20 μg/ml propofol significantly increased the expression of activated Drp1 (pDrp1 Ser 616). The data are presented as a ratio of pDrp1/total Drp1 and as a percentage of the control (B) Western blotting was also used to assess the expression of mitofusion 1 and 2 (MFN1 and MFN2) and optic atrophy 1 (OPA1), proteins all responsible for inducing mitochondrial fusion (a). After 6 h of exposure to 20 μg/ml propofol, there was no significant change in the expression of MFN1, MFN2, or OPA1 compared with control-treated cells (b–d), indicating that propofol exposure does not significantly affect mitochondrial fusion. These data are presented as a percentage of the control group following normalization to COX IV, a marker of the inner mitochondrial membrane. (**P < 0.01, n = 5 per group.) NS = Not significant.

Exposure of human embryonic stem cell–derived neurons to propofol altered the expression of the mitochondrial fission-related protein and did not affect mitochondrial fusion. (A) Western blotting was used to assess the expression of dynamin-related protein 1 (Drp1), a protein responsible for inducing mitochondrial fission. Drp1 becomes activated when phosphorylated at the Ser616 position. Exposure of human embryonic stem cell–derived neurons to 6 h of 20 μg/ml propofol significantly increased the expression of activated Drp1 (pDrp1 Ser 616). The data are presented as a ratio of pDrp1/total Drp1 and as a percentage of the control (B) Western blotting was also used to assess the expression of mitofusion 1 and 2 (MFN1 and MFN2) and optic atrophy 1 (OPA1), proteins all responsible for inducing mitochondrial fusion (a). After 6 h of exposure to 20 μg/ml propofol, there was no significant change in the expression of MFN1, MFN2, or OPA1 compared with control-treated cells (bd), indicating that propofol exposure does not significantly affect mitochondrial fusion. These data are presented as a percentage of the control group following normalization to COX IV, a marker of the inner mitochondrial membrane. (**P < 0.01, n = 5 per group.) NS = Not significant.

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