Controlling Redox Status for Stem Cell Survival, Expansion, and Differentiation

Figure 2

Regulation of stem cell proliferation and survival by ROS. (a) Effect of physiological levels of ROS. Physiological levels of ROS activate various MAPKs (i.e., ERK, p38, and AKT), promoting stem cell proliferation. Mir-210 is upregulated by ROS and is also involved in the MAPK activation, leading to the enhanced stem cell proliferation. Mild levels of ROS promote the activation of pATM, increasing the DNA stability of stem cells. Mild ROS can sustain antibacterial properties of PSCs and the proangiogenic functions of MSCs. (b) Effect of excessive levels of ROS. Excessive levels of ROS induce oxidative stress in stem cells. High levels of ROS result in a decreased stem cell adhesion (i.e., through a decreased activation of FAK-Src signaling) and proliferation (through the reduced activation of pRB). High ROS also reduce DNA stability and induce apoptosis (in favoring BAX-BAK dimerization and the formation of channel facilitating cytochrome c (cyt c) cytoplasmic translocation). In (a), Cyt c red means Cyt c reductase.

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