Abstract
Background & Aim Stem cell-based treatment for tissue regeneration requires millions of cells. Repeated subculture is required for the expansion of these cells, and this is often complicated by senescence. Senescence reduces the cellular activity and function of stem cells and inhibits the potential of these cells to regenerate ischemic tissue. Therefore, novel strategies are required to enhance the function of stem cells and attenuated senescence. Oxidative stress activates stem cell senescence. During reperfusion and following myocardial infarction, oxidative stress rapidly increases in the heart leading to cardiac remodeling. Excessive ROS induces apoptosis and impairs normal cellular function. Therefore, the reduction of excessive ROS ameliorates functional impairment and prevents cardiac remodeling. Thus, numerous antioxidants are reported to have cardio-protective effects. In the present study, I have identified MHY-1685 as a new antioxidant, which also inhibits senescence. I investigated MHY-1685’s effect on the cellular activities of hCPCs such as proliferation, differentiation, clonogenicity, and paracrine effects, I evaluated the therapeutic potential of MHY-1685 as a priming agent for hCPCs in an in vivo myocardial infarction model. Methods, Results & Conclusion Continuous treatment with MHY-1685(M5) delayed cellular senescence in hCPCs and showed antioxidant and anti-apoptotic effects under oxidative stress conditions. M5 increased the capacity of in vitro hCPCs to proliferate and form tubes, to differentiate into smooth muscle cells, and to form colonies. Furthermore, M5 was found to enhance these functions in senescent hCPCs that were transplanted into a rat MI model. Moreover, M5-primed hCPCs increased capilary density in the infarct (117.6±15.4 in M5-treated hCPCs,56.8±9.9 in control group)and border zones(270.8±13.6 in M5-treated hCPCs, 216.5±23.6 in the control group; p In conclusion, these studies present effective strategies for the development of CPCs-based therapy for myocardial infarction.
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