May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Caloric Restriction Reduces Caspase–1 Induced Photoreceptor Apoptosis After Bright Light Exposure
Author Affiliations & Notes
  • M. griffin
    Biology, Boston College, Chestnut Hill, MA
  • J. Chalifoux
    Biology, Boston College, Chestnut Hill, MA
  • G. Gressel
    Biology, Boston College, Chestnut Hill, MA
  • A. Johnson
    Biology, Boston College, Chestnut Hill, MA
  • R. Hurst
    Biology, Boston College, Chestnut Hill, MA
  • W.J. Brunken
    Anatomy and Cellular Biology, Tufts University School of Medicine, Boston, MA
  • G.W. Balkema
    Biology, Boston College, Chestnut Hill, MA
  • Footnotes
    Commercial Relationships  M. griffin, None; J. Chalifoux, None; G. Gressel, None; A. Johnson, None; R. Hurst, None; W.J. Brunken, None; G.W. Balkema, None.
  • Footnotes
    Support  NEI–R01 EY12676, NEI–P30 EY13078, NSF–0417843
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 4824. doi:
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      M. griffin, J. Chalifoux, G. Gressel, A. Johnson, R. Hurst, W.J. Brunken, G.W. Balkema; Caloric Restriction Reduces Caspase–1 Induced Photoreceptor Apoptosis After Bright Light Exposure . Invest. Ophthalmol. Vis. Sci. 2006;47(13):4824.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Bright light damage has been shown to increase photoreceptor (PR) apoptosis in the retina. Caloric restriction (CR) has been shown to protect photoreceptors from age–related cell death. Here, we test the hypothesis that CR protects photoreceptors from light–damage. After establishing a protective effect, we sought to determine whether the protection results from an anti–apoptotic effect or an increase in neurogenesis.

Methods: : Caloric intake was reduced in adult black (+/+) and congenic albino (C2J) mice by an amount sufficient to lower body weight to 85% of ad libidum (AL) weight. Retinas were collected from mice fed under CR or AL regimes; animals were housed in dim (10–2 cd/m2) or bright (1000 cd/m2) lighting conditions on a 12:12 light:dark cycle. To test for neurogenesis, a subset of mice from all conditions was injected (IP) with BrdU 2 days after the induction of light damage. Radial sections of retinas were examined by conventional histology. The changes in expression of Caspase–1, Caspase–3, and Sirt1, and the incorporation of BrdU were examined using immunohistochemical methods.

Results: : Increased numbers of photoreceptors were present in CR mice compared to AL mice suggesting that CR protected photoreceptors from light–induced cell death. Moreover, CR reduced the number of TUNEL–positive cells in all conditions. In parallel with the decreased TUNEL labeling, Caspase–1 expression was also reduced. Caspase–3 expression was too low in all conditions to allow for any interpretation. Sirt1 expression was also unchanged among these conditions. A small number of BrdU–positive cells were observed in the bright light conditions, but not in dim light conditions. These cells rarely incorporated into the photoreceptor layer. BrdU–labeling was independent of feeding conditions.

Conclusions: : The data together suggest that the major effect of caloric restriction is to reduce light–induced apoptosis. Modulation of the caspase–1 pathway appears to mediate this protective effect, while caspase–3 and sirt1 have no observable role. In parallel, light damage increases cell proliferation; feeding regimes appear to have no effect on this induction.

Keywords: neuroprotection • radiation damage: light/UV • photoreceptors 

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