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Mitochondrial Dysfunction in a High Intraocular Pressure-Induced Retinal Ischemia Minipig Model
Michael Pasák1, Marie Vanišová1, Lucie Tichotová2
1Laboratory for Study of Mitochondrial Disorders, Department of Paediatrics and Inherited Metabolic Disorders, First Faculty of Medicine, Charles University and General University Hospital in Prague, 12801 Prague, Czech Republic.
Biomolecules
|October 27, 2022
Summary
Mitochondrial dysfunction occurs in retinal ischemia (RI). This study used a minipig model to show changes in mitochondrial parameters in the retina and RPE, suggesting RI models are useful for studying mitochondrial damage.
Area of Science:
- Ophthalmology
- Mitochondrial Biology
- Neuroscience
Background:
- Retinal ischemia (RI) and progressive neuronal death threaten vision.
- Mitochondrial dysfunction and altered fusion/fission dynamics are implicated in RI pathophysiology.
Purpose of the Study:
- To investigate changes in mitochondrial parameters within the neuroretina, retinal pigment epithelium (RPE), and choroid.
- To utilize a porcine high intraocular pressure (IOP)-induced RI minipig model.
Main Methods:
- Induced acute IOP elevation in one eye of minipigs, comparing it to the control eye.
- Analyzed respiratory chain complex (RCC) activity and amount, Coenzyme Q10 (CoQ10) content, mitochondrial ultrastructure, and mt-pathway gene expression.
Main Results:
- Increased RCC I activity and decreased CoQ10 content were observed in RPE cells.
- CORE2 (RCC III subunit) and DRP1 protein levels were significantly decreased in the neuroretina.
- Expression of mt-quality control genes *Drp1* and *Opa1* decreased in RPE and neuroretina.
Conclusions:
- The minipig eye serves as a viable model for studying mitochondrial dysfunction in RI.
- Mitochondrial protective strategies may mitigate acute damage and delay the onset of RI.
