April 2009
Volume 50, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2009
Elevated Apo A1 Protects Against Dietary Fat Induced Retinal Apoptosis in C57BL6/J Mice
Author Affiliations & Notes
  • S. M. Porter
    Ophthalmology, UC Davis, Davis, California
  • C. J. Park
    Ophthalmology, UC Davis, Davis, California
  • D. Karkazis
    Ophthalmology, UC Davis, Davis, California
  • S. Oltjen
    Ophthalmology, UC Davis, Davis, California
  • K. Forward
    Ophthalmology, UC Davis, Davis, California
  • L. Hjelmeland
    Ophthalmology, UC Davis, Davis, California
  • L. S. Morse
    Ophthalmology, UC Davis, Davis, California
Investigative Ophthalmology & Visual Science April 2009, Vol.50, 2978. doi:
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    • Get Citation

      S. M. Porter, C. J. Park, D. Karkazis, S. Oltjen, K. Forward, L. Hjelmeland, L. S. Morse; Elevated Apo A1 Protects Against Dietary Fat Induced Retinal Apoptosis in C57BL6/J Mice. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2978.

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

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Abstract

Purpose: : To investigate the effect of dietary fat and age on retinal apoptosis in a mouse model.

Methods: : All animals were treated according to ARVO guidelines for animal care. C57BL6/J mice and a Tg-Apo A-1 genetic variant with the same genetic background were used in the following groups: Group 1: young mice (8 wk old ; n= 4); old mice (16 month old; n = 4); Tg Apo A-1 young mice (8 wk old; n = 4); were fed normal diet (5% fat). Group 2: young (8 wks; n=4); old mice (16 month old, n=4), young Tg Apo A-1 (8 wk old, n=4); were fed high fat Paigen diet (15% fat/1.25% cholesterol). After 4 months of feeding serum cholesterol levels were obtained, animals were euthanized with pentobarbital and eyes were harvested and sectioned. Retinas were fixed in 0.5% gluataraldehyde. The TUNEL assay (Millipore ApoTag) was performed to detect apoptosis followed by DAPI counter stain to detect retinal nuclei. 12 different and evenly dispersed high power fields were evaluated for each animal. The total number of apoptotic cells and total number of nuclei were recorded per high power field. The percent of apoptosis was then calculated and the data analyzed by ANOVA.

Results: : The Paigen diet showed marked increase in serum cholesterol levels in both young and old animals fed the diet. Regardless of diet, the Tg Apo A-1 mice displayed marked elevation in serum HDL cholesterol levels compared to normal C57BL6/J mice. Apoptosis assays revealed the following: Group 1: normal diet: percent apoptosis: 0.022 young; 0.04 for aged animals; 0.0048 young Tg Apo A-1.Group 2: Paigen high fat diet: 0.102 young animals; 0.1056 aged animals; 0.026 young Tg Apo A-1 animals. All values are statistically significant at P= 0.0001.

Conclusions: : Increased dietary fat lead to statistically significant increase in the rate of apoptosis in all groups. However, the percent of apoptosis is significantly less in the Tg Apo A-1 mice compared to young normal C57BL6/J mice fed the same diet. The enhanced reverse cholesterol transport inherent to the Tg mice may confer a protective mechanism against apoptosis in the mouse model. This has interesting implications for the intervention or prevention of atrophic AMD.

Keywords: apoptosis/cell death • age-related macular degeneration • lipids 
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