Mitochondria-targeted peptide MTP-131 alleviates mitochondrial dysfunction and oxidative damage in human trabecular meshwork cells.

@article{Chen2011MitochondriatargetedPM,
  title={Mitochondria-targeted peptide MTP-131 alleviates mitochondrial dysfunction and oxidative damage in human trabecular meshwork cells.},
  author={Min Chen and Bing-qian Liu and Qianying Gao and Yehong Zhuo and Jian Ge},
  journal={Investigative ophthalmology \& visual science},
  year={2011},
  volume={52 10},
  pages={
          7027-37
        }
}
PURPOSE To investigate the antioxidative ability of a novel mitochondria-targeted peptide MTP-131 in immortalized human trabecular meshwork (iHTM) and glaucomatous human trabecular meshwork (GTM(3)) cell lines. METHODS Cultured iHTM and GTM(3) cells were pretreated with MTP-131 for 1 hour, and sustained oxidative stress was induced by subjecting TM cells to 200 μM hydrogen peroxide (H(2)O(2)) for 24 hours. Untreated cells and cells incubated with H(2)O(2) alone were used as controls. Lactate… 

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References

SHOWING 1-10 OF 44 REFERENCES

Mitochondria-targeted cytoprotective peptides for ischemia-reperfusion injury.

  • H. Szeto
  • Biology
    Antioxidants & redox signaling
  • 2008
TLDR
A novel class of cell-permeable small peptides (Szeto-Schiller peptides) that selectively partition to the inner mitochondrial membrane and possess intrinsic mitoprotective properties are focused on.

Sustained stress response after oxidative stress in trabecular meshwork cells

TLDR
Chronic oxidative stress in TM cells induced iROS production in mitochondria, which may contribute to the pathogenesis of the TM in glaucoma by inducing the expression of inflammatory mediators previously observed in glAUcoma donors as well as the levels of oxidative damage in the tissue.

Cell-permeable Peptide Antioxidants Targeted to Inner Mitochondrial Membrane inhibit Mitochondrial Swelling, Oxidative Cell Death, and Reperfusion Injury*

TLDR
Overproduction of ROS underlies the cellular toxicity of tBHP and 3NP, and ROS mediate cytochrome c release via MPT, and these IMM-targeted antioxidants may be very beneficial in the treatment of aging and diseases associated with oxidative stress.

Mitochondrial defects and dysfunction in calcium regulation in glaucomatous trabecular meshwork cells.

TLDR
POAG TM cells have defective mitochondrial function, which causes them to be abnormally vulnerable to Ca(2+) stress, and pharmacologic inhibitors of IP3R, MPTP opening, and cyclophilin D could have clinical implications for primary open-angle glaucoma.

Mitochondria-targeted peptide antioxidants: Novel neuroprotective agents

TLDR
The development of a novel class of mitochondria-targeted antioxidants that can protect mitochondria against oxidative stress and prevent neuronal cell death in animal models of stroke, Parkinson’s disease, and amyotrophic lateral sclerosis is summarized.

Mitochondrial complex I defect induces ROS release and degeneration in trabecular meshwork cells of POAG patients: protection by antioxidants.

  • Yuan HeK. Leung J. Ge
  • Biology, Medicine
    Investigative ophthalmology & visual science
  • 2008
TLDR
It is proposed that a mitochondrial complex I defect is associated with the degeneration of TM cells in patients with POAG, and antioxidants and MPT inhibitors can reduce the progression of this condition.

Do mitochondriotropic antioxidants prevent chlorinative stress-induced mitochondrial and cellular injury?

TLDR
It is shown that recently developed mitochondria-targeted antioxidants (MitoQ and SS31) significantly protected against HOCl-induced mitochondrial damage and cell death at concentrations >or=25 nM.

Mitochondria, oxidative stress and cell death

TLDR
There is accumulating evidence supporting a direct link between mitochondria, oxidative stress and cell death.