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Published on: June 2, 2019
AGGF1-primed endothelial progenitor cells alleviate ischaemia-reperfusion injury in diabetic hearts
Xia Li1,2, Suwan Mu1,3, Shuting Huang1,3
1Department of Cell Biology and Genetics, School of Intelligent Medicine and Biotechnology, Guilin Medical University, ZhiYuan Road #1, Guilin, Guangxi, China.
Insights
AGGF1 protein protects endothelial progenitor cells (EPCs) from damage caused by high glucose and hypoxia/reoxygenation. AGGF1-EPCs therapy improves cardiac function and reduces oxidative stress in diabetic ischemia-reperfusion injury.
Area of Science:
- Cardiovascular Research
- Regenerative Medicine
- Diabetology
Background:
- Cardioprotective agents often fail in diabetic hearts.
- The protective mechanisms of AGGF1 on endothelial progenitor cells (EPCs) under diabetic stress are not well understood.
Purpose of the Study:
- To investigate the role of AGGF1 in protecting EPCs from hyperglycemia (HG) and hypoxia/reoxygenation (H/R) stress.
- To evaluate the efficacy of AGGF1-EPCs therapy in a mouse model of diabetic ischemia-reperfusion (I/R) injury.
Main Methods:
- Assessed the protective effects of AGGF1 on EPCs exposed to HG + H/R conditions.
- Administered AGGF1-EPCs therapy to diabetic I/R mice.
- Measured cardiac function, reactive oxygen species (ROS) production, and fibrosis.
- Investigated the molecular mechanism involving Nrf2 activation.
Main Results:
- AGGF1 abolished the damaging effects of HG + H/R on EPCs.
- AGGF1-EPCs therapy restored cardiac function and inhibited ROS production and fibrosis in diabetic I/R mice.
- AGGF1 activated the Nrf2 pathway, leading to the induction of antioxidative proteins (HO1, NQO1, CAT).
Conclusions:
- AGGF1 protein protects EPCs from HG + H/R-induced damage via the antioxidative Nrf2 pathway.
- AGGF1-EPCs therapy represents a promising novel strategy for treating diabetic I/R injury.
Abstract:
A number of cardioprotective pharmacological agents are not effective in diabetic hearts. The role of AGGF1-EPCs therapy in diabetic ischaemia-reperfusion(I/R) injury and the underlying mechanism by which AGGF1 regulates EPCs under hyperglycemia (HG) + hypoxia/reoxygenation (H/R) stress are still unclear. We observed that the damaging effects of HG + H/R on EPCs were abolished by AGGF1. The EPCs implantation therapy successfully restores cardiac functions, inhibits ROS production and fibrosis in diabetic I/R mice. Mechanistically, AGGF1 activates the Nrf2 and induces the activation of downstream antioxidative proteins (HO1, NQO1, and CAT). These data suggest that AGGF1 protein reverses the damaging effects of HG + H/R on EPCs via the antioxidative Nrf2. AGGF1-EPCs therapy is a novel strategy for treating diabetic I/R injury.
