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Mitochondrial morphology differences and mitophagy deficit in murine glaucomatous optic nerve
Lucy Coughlin1, Richard S Morrison2, Philip J Horner2
1Department of Pharmaceutical Sciences, Northeast Ohio Medical University, Rootstown, Ohio, United States School of Biomedical Sciences, Kent State University, Kent, Ohio, United States.
Investigative Ophthalmology & Visual Science
|February 7, 2015
Summary
Mitochondrial pathology in the optic nerve contributes to energy deficits in glaucoma. In DBA/2J mice, increased, smaller mitochondria and impaired recycling suggest disease progression.
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Glaucoma is characterized by optic nerve damage and ATP depletion.
- Mitochondrial dysfunction is implicated in the energy deficit observed in glaucomatous optic nerves.
Purpose of the Study:
- To investigate mitochondrial morphology and health in the optic nerve axons of DBA/2J mice, a model for glaucoma.
- To understand the underlying causes of energy deficits in glaucomatous optic nerves.
Main Methods:
- Mitochondrial dimensions and health were assessed using electron microscopy in DBA/2J and control mice at various ages.
- Western blot analysis was performed on optic nerve protein to examine levels of key proteins involved in mitochondrial dynamics and mitophagy (PINK1, Parkin, LC3, LAMP1).
Main Results:
- DBA/2J mice exhibited an increased number of smaller, more disrupted mitochondria in their optic nerves compared to controls.
- Autophagosomes were elevated, but lysosome-associated membrane protein 1 (LAMP1) levels were decreased, suggesting inefficient mitophagy.
- While LC3-II/LC3-I ratios increased with age, PINK1 and Parkin levels showed no significant differences.
Conclusions:
- Mitochondrial pathology, characterized by reduced surface area and oxidative capacity, likely contributes to the energy deficit in glaucomatous optic nerves.
- Increased autophagosomes coupled with decreased LAMP1 indicate impaired mitochondrial recycling (mitophagy) in DBA/2J mice.
- These findings highlight mitochondrial dysfunction and inefficient mitophagy as key factors in glaucoma pathogenesis.
