May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Ultrastructural Changes Originated by Aging, High–Fat Diet and APO–E Deficiency in Mouse RPE and Bruch’s Membrane
Author Affiliations & Notes
  • P. Fernandez
    Experimental Ophthalmology Laboratory, University of Navarra, Pamplona Navarra, Spain
  • L.M. Sadaba
    Ophthalmology, University Clinic, Pamplona Navarra, Spain
  • J. Moreno–Montañes
    Ophthalmology, University Clinic, Pamplona Navarra, Spain
  • A. Garcia–Layana
    Ophthalmology, University Clinic, Pamplona Navarra, Spain
  • Footnotes
    Commercial Relationships  P. Fernandez, None; L.M. Sadaba, None; J. Moreno–Montañes, None; A. Garcia–Layana, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1593. doi:
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      P. Fernandez, L.M. Sadaba, J. Moreno–Montañes, A. Garcia–Layana; Ultrastructural Changes Originated by Aging, High–Fat Diet and APO–E Deficiency in Mouse RPE and Bruch’s Membrane . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1593.

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

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Abstract: : Purpose: ApoE–/– deficient mouse (apoE–/–), experimental model of genetic hypercholesterolemia, develops atherosclerosis and shows ultrastructural retinal alterations. Several systemic and ocular pathologies have been also associated with aging and a fat increase in diet. We investigated the effect of these risk factors in mouse retinal pigment epithelium (RPE) and Bruch's Membrane (BM). Methods: Eighteen mice were divided into six groups (n=3): WT: C57BL/6 with standard chow (SC, 6 months); AE: apoE–/– with SC (6 months); WTHC: C57BL/6 with high fat/cholesterol chow (HC, 12 months); WTO: C57BL/6 with SC (25 months); AEHC: apoE–/– with HC (12 months); AEOHC: apoE–/– with HC (23 months). The duration of HC supplementation was 3 months. All mice were perfunded with paraformaldehyde 4% and eyecups dissected to be processed for transmission electron microscopy. Results: Electron micrographs showed that morphology of WT group was normal. The rest of the groups showed alterations such as developing of empty, lipidic and autophagocytic vacuoles (grading: AEOHC>AEHC=WTHC>AE=WTO), basal laminar deposits (BLD) formation (AEOHC>WTO>WTHC=AE>AEHC) and nuclear pyknosis and nuclear membrane alteration (AEOHC>AEHC=WTHC>WTO=AE). In group WTO there was also patent sprouting in choriocapillaries and observation of basal lineal deposits (BLinD). In summary, dietetic hypercholesterolemia, mainly produced severe nuclear alterations and severe vacuolization in RPE cells combined with small solitary patches of BLD. Genetic hypercholesterolemia, induced moderate vacuolization and increased amount of BLD. Aging mostly produced an increase in BLD and formation of BlinD and sprouting induction. As we expected, the combination of all risk factors produced nuclear and cytoplasm alterations with the highest severity and intensity. Conclusions: In this study we have reported several differences in ultrastructural alterations caused by aging, dietetic and genetic hypercholesterolemia and the combination of some of these conditions. We speculate that oxidative stress (hypercholesterolemia or aging–derived) would be involved, at least in part, of these alterations, comparable with those seen in early stages of retinal diseases. However more studies will be performed to confirm this hypothesis.

Keywords: retinal pigment epithelium • Bruch's membrane • microscopy: electron microscopy 

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