April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
Mitochondria-targeted Peptide Mtp-131 Alleviates Mitochondrial Dysfunction And Oxidative Damage In Human Trabecular Meshwork Cells
Author Affiliations & Notes
  • Jian Ge
    Glaucoma, Zhongshan Ophthalmic Center, Guangzhou, China
  • Min Chen
    Glaucoma, Zhongshan Ophthalmic Center, Guangzhou, China
  • Bingqian Liu
    Glaucoma, Zhongshan Ophthalmic Center, Guangzhou, China
  • Qianying Gao
    Glaucoma, Zhongshan Ophthalmic Center, Guangzhou, China
  • Yehong Zhuo
    Glaucoma, Zhongshan Ophthalmic Center, Guangzhou, China
  • Footnotes
    Commercial Relationships  Jian Ge, None; Min Chen, None; Bingqian Liu, None; Qianying Gao, None; Yehong Zhuo, None
  • Footnotes
    Support  The National Basic Research Program of China 2007CB512200
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 5923. doi:
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      Jian Ge, Min Chen, Bingqian Liu, Qianying Gao, Yehong Zhuo; Mitochondria-targeted Peptide Mtp-131 Alleviates Mitochondrial Dysfunction And Oxidative Damage In Human Trabecular Meshwork Cells. Invest. Ophthalmol. Vis. Sci. 2011;52(14):5923.

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Abstract
 
Purpose:
 

To investigate the anti-oxidative ability of a novel cell-penetrating,mitochondria-targeted peptide MTP-131 in glaucomatous humantrabecular meshwork (GTM3) and immortalized human trabecularmeshwork (iHTM) cell lines.

 
Methods:
 

Cultured iHTM and GTM3 cells were pretreated with MTP-131 for1 h, and then sustained oxidative stress was applied by subjectingTM cells to 200µM hydrogen peroxide (H2O2) for 24 h. Untreatedcells and cells incubated with H2O2 alone were used as controls.Lactate dehydrogenase (LDH) assay was used to determine cellviability. Changes of mitochondrial membrane potential (ΔΨm) andgeneration of intracellular reactive oxygen species (ROS) wereused to analyze mitochondrial functions by flow cytometry andconfocal microscopy. Apoptosis was quantified by flow cytometry,activation of caspase 3 was quantified with western blot, andrelease of cytochrome c and changes in cytoskeleton was analyzedwith confocal.

 
Results:
 

In both iHTM and GTM3 cells, sustained oxidative stress inducedby H2O2 resulted in a decrease in ΔΨm and elevation of intracellularROS. When cells were pretreated with MTP-131, the H2O2-inducedmitochondrial depolarization was prevented; intracellular ROS,LDH release and apoptosis was significantly decreased; releaseof cytochrome c from mitochondria to cytoplasm and activationof caspase 3 was inhibited. In addition, cytoskeleton changescaused by chronic oxidative stress were also alleviated by MTP-131.

 
Conclusions:
 

Mitochondria-targeted peptide MTP-131 could prevent both iHTMand GTM3 cells from sustained oxidative stress induced by H2O2.  

 

 
Keywords: mitochondria • neuroprotection 
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