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Updated: Apr 7, 2026
Near Infrared NIr Light Increases Expression of a Marker of Mitochondrial Function in the Mouse Vestibular Sensory Epithelium
Published on: March 14, 2015
Mitochondrial decline precedes phenotype development in the complement factor H mouse model of retinal degeneration
Karin C Calaza1, Jaimie Hoh Kam2, Chris Hogg3
1Program of Neurosciences, Institute of Biology, Federal Fluminense University, Rio de Janeiro, Brazil; Institute of Ophthalmology University College London, London, UK.
Abstract:
Mitochondria produce adenosine triphosphate (ATP), critical for cellular metabolism. ATP declines with age, which is associated with inflammation. Here, we measure retinal and brain ATP in normal C57BL/6 and complement factor H knockout mice (Cfh(-/-)), which are proposed as a model of age-related macular degeneration. We show a significant premature 30% decline in retinal ATP in Cfh(-/-) mice and a subsequent shift in expression of a heat shock protein that is predominantly mitochondrial (Hsp60). Changes in Hsp60 are associated with stress and neuroprotection. We find no differences in brain ATP between C57BL/6 and Cfh(-/-) mice. Near infrared (NIR) increases ATP and reduces inflammation. ATP decline in Cfh(-/-) mice was corrected with NIR which also shifted Hsp60 labeling patterns. ATP decline in Cfh(-/-) mice occurs before inflammation becomes established and photoreceptor loss occurs and may relate to disease etiology. However, ATP levels were corrected with NIR. In summary, we provide evidence for a mitochondrial basis for this disease in mice and correct this with simple light exposure known to improve mitochondrial function.
Insights
Mitochondrial adenosine triphosphate (ATP) decline in a mouse model of age-related macular degeneration was reversed by near-infrared light. This light therapy improved retinal ATP levels and mitochondrial stress markers.
Area of Science:
- Mitochondrial biology
- Neuroscience
- Ophthalmology
Background:
- Mitochondria are vital for cellular energy production through adenosine triphosphate (ATP).
- Age-related decline in ATP is linked to inflammation and cellular dysfunction.
- Complement factor H knockout mice serve as a model for age-related macular degeneration (AMD).
Purpose of the Study:
- To investigate retinal and brain ATP levels in a mouse model of AMD.
- To explore the therapeutic potential of near-infrared (NIR) light on mitochondrial function and inflammation in this model.
Main Methods:
- Measurement of retinal and brain ATP levels in C57BL/6 and Cfh(-/-) mice.
- Analysis of heat shock protein 60 (Hsp60) expression as a mitochondrial stress marker.
- Application of near-infrared (NIR) light therapy to Cfh(-/-) mice.
Main Results:
- A significant 30% premature decline in retinal ATP was observed in Cfh(-/-) mice.
- NIR therapy successfully corrected the retinal ATP decline and altered Hsp60 expression patterns.
- No differences in brain ATP were found between the mouse groups.
Conclusions:
- Mitochondrial dysfunction, indicated by ATP decline, may underlie AMD pathogenesis.
- NIR light therapy demonstrates potential for improving mitochondrial function and addressing AMD.
- Early ATP decline precedes inflammation and photoreceptor loss in the AMD mouse model.
