Palmitic Acid Methyl Ester Induces G₂/M Arrest in Human Bone Marrow-Derived Mesenchymal Stem Cells via the p53/p21 Pathway

Figure 4

Involvement of the p53-p21 pathway and ROS in the PAME-induced G₂/M cell cycle arrest in hBM-MSCs. Treatment with PAME (50 μM) for 48 h increased the protein levels of (a) p53 () and (b) p21 (), but not (c) Cdc25C (). (d) PAME did not significantly affect the level of mitochondrial ROS. The top panel shows that the mitochondrial ROS was detected by flow cytometric analysis using MitoSOX™ Red reagent; the bottom panel shows a graph of quantitation of these data. AMA-treated hBM-MSCs were used as a positive control for mitochondrial ROS production (). (e) PAME did not significantly affect the level of cytosolic ROS. H₂O₂-treated hBM-MSCs served as a positive control for cytosolic ROS production. The top panel shows ROS image detected by confocal microscopy using CM-H₂DCFDA; the bottom panel shows a graph of quantitation of these data. At least 20 cells from 2 randomly selected fields were scored in each experiment to determine the DCFDA intensity (). All data represent . , versus the control group. AMA: antimycin A.

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