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Experimental Autoimmune Uveitis: An Intraocular Inflammatory Mouse Model
Published on: January 12, 2022
Mitochondrial proteomics in experimental autoimmune uveitis oxidative stress
Sindhu Saraswathy1, Narsing A Rao
1Doheny Eye Institute, Department of Ophthalmology, Keck School of Medicine of the University of Southern California, Los Angeles, California 90033, USA.
Investigative Ophthalmology & Visual Science
|July 7, 2009
Summary
Early experimental autoimmune uveitis (EAU) involves photoreceptor mitochondrial oxidative stress, altering retinal protein levels. Key proteins like manganese-SOD and alphaA crystallin increase, while ATP synthase decreases, indicating early retinal damage without apoptosis.
Area of Science:
- Ophthalmology
- Immunology
- Mitochondrial Biology
Background:
- Photoreceptor mitochondrial oxidative stress initiates experimental autoimmune uveitis (EAU).
- Understanding early protein alterations in the retina during EAU is crucial for identifying pathogenic mechanisms.
Purpose of the Study:
- To determine changes in retinal mitochondrial protein levels during the early phase of EAU.
- To investigate the role of oxidative stress in early EAU pathogenesis.
Main Methods:
- Retinal mitochondrial fractions from early EAU were analyzed using 2D-DIGE.
- Differential protein expression was identified by MALDI-TOF MS.
- Protein and mRNA levels were confirmed by Western blot and real-time PCR, respectively.
Main Results:
- 13 proteins showed differential expression; 10 were upregulated (e.g., manganese-SOD, alphaA crystallin) and 4 downregulated (e.g., ATP synthase, malate dehydrogenase).
- Western blot and qPCR confirmed increased levels of alphaA crystallin, betaB2 crystallin, MnSOD, and Hsp70, and decreased ATP synthase.
- Apoptosis was not detected in the early stages of EAU.
Conclusions:
- Upregulated mitochondrial oxidative stress proteins and downregulated ATP synthase suggest early retinal damage in EAU.
- Elevated mitochondrial alphaA and betaB2 crystallin may offer protection against cell death in early EAU.
