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Maintaining mitochondrial membrane impermeability. an opportunity for new therapy in glaucoma?

W G Tatton1, R M Chalmers-Redman, A Sud

  • 1Departments of Ophthalmology, Mount Sinai School of Medicine, New York, NY 10029, USA. william.tatton@mssm.edu

Survey of Ophthalmology
|May 30, 2001
PubMed

Insights

Mitochondrial apoptosis contributes to retinal ganglion cell loss in glaucoma. Akt signaling and anti-apoptotic proteins like BCL-2 protect these cells by regulating mitochondrial permeability.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Neuroscience

Background:

  • Apoptosis, or programmed cell death, is implicated in retinal ganglion cell (RGC) loss in glaucoma.
  • Mitochondria-dependent apoptosis signaling pathways are increasingly recognized in glaucoma models with elevated intraocular pressure.
  • This process involves increased mitochondrial membrane permeability and the release of pro-apoptotic factors.

Purpose of the Study:

  • To investigate the role of mitochondrially dependent apoptosis in RGC loss in a rat glaucoma model.
  • To explore the function of anti-apoptotic proteins and Akt signaling in protecting RGCs from apoptosis.

Main Methods:

  • Utilized a rat model of glaucoma with induced chronic intraocular pressure.
  • Examined mitochondrial membrane permeability and the role of the mitochondrial megapore.
  • Investigated the involvement of BCL-2, BCL-X(L), and phosphorylated Akt (protein kinase B) in RGC survival.

Main Results:

  • Mitochondrial megapore opening contributes to increased mitochondrial membrane permeability during apoptosis.
  • Anti-apoptotic proteins BCL-2 and BCL-X(L) bind to the megapore, promoting its closure and reducing permeability.
  • Phosphorylated Akt integrates survival signals, enhancing the protective effects of BCL-2 and BCL-X(L) against apoptotic insults.

Conclusions:

  • Mitochondria-dependent apoptosis is a key mechanism in RGC loss in glaucoma.
  • Akt signaling pathways, in conjunction with BCL-2 and BCL-X(L), offer a protective mechanism for RGCs.
  • Targeting these pathways with agents like brimonidine and propargylamines may represent a therapeutic strategy for glaucoma.

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