H2O2-Activated Mitochondrial Phospholipase iPLA2γ Prevents Lipotoxic Oxidative Stress in Synergy with UCP2, Amplifies Signaling via G-Protein–Coupled Receptor GPR40, and Regulates Insulin Secretion in Pancreatic β-Cells

@inproceedings{Jeek2015H2O2ActivatedMP,
  title={H2O2-Activated Mitochondrial Phospholipase iPLA2γ Prevents Lipotoxic Oxidative Stress in Synergy with UCP2, Amplifies Signaling via G-Protein–Coupled Receptor GPR40, and Regulates Insulin Secretion in Pancreatic β-Cells},
  author={Jan Je{\vz}ek and Andrea Dlaskov{\'a} and Jaroslav Zelenka and Martin Jabůrek and Petr Jezek},
  booktitle={Antioxidants & redox signaling},
  year={2015}
}
AIMS Pancreatic β-cell chronic lipotoxicity evolves from acute free fatty acid (FA)-mediated oxidative stress, unprotected by antioxidant mechanisms. Since mitochondrial uncoupling protein-2 (UCP2) plays antioxidant and insulin-regulating roles in pancreatic β-cells, we tested our hypothesis, that UCP2-mediated uncoupling attenuating mitochondrial superoxide production is initiated by FA release due to a direct H2O2-induced activation of mitochondrial phospholipase iPLA2γ. RESULTS Pro-oxidant… CONTINUE READING

Citations

Publications citing this paper.
SHOWING 1-8 OF 8 CITATIONS

Potential of Mitochondria-Targeted Antioxidants to Prevent Oxidative Stress in Pancreatic β-cells

  • Oxidative medicine and cellular longevity
  • 2019
VIEW 9 EXCERPTS
CITES METHODS & BACKGROUND
HIGHLY INFLUENCED

References

Publications referenced by this paper.
SHOWING 1-10 OF 53 REFERENCES

Similar Papers

Loading similar papers…