[Expression of nitric oxide synthases in the retina of OXYS rats during retinopathy development]

Adv Gerontol. 2014;27(1):87-93.
[Article in Russian]

Abstract

Both the lack and excess generation of nitric oxide (NO) contributes to the pathogenesis of age-related diseases, according to the latest data including age-related macular degeneration (AMD), which is a leading cause of vision loss in people over 65. The mechanisms of the effects of NO are not entirely clear, the information about changes in the expression synthase NO (NOSs) in the retina with age and the development of AMD are limited. We showed previously that the senescence-accelerated OXYS rats strain is an animal model of AMD. The purpose of the present research was to compare the transcriptional activity of genes NOSs: neuronal (nNOS), inducible (iNOS) and endothelial (eNOS) in the retina OXYS and Wistar rats (used as control) by real-time PCR. The study was carried out on animals at the age of 3 and 18 months during the period of manifestation and active progression of AMD-like retinopathy in OXYS rats. We showed that mRNA level of NOSs was not dependent on age in Wistar and OXYS rats. Interstrain differences in the level of eNOS mRNA were not detected, but the level of mRNA of nNOS in the retina of 18-month-old OXYS rats was 2,4 times higher than in age-matched Wistar rats. Regardless of age the level of iNOS mRNA in OXYS rats was 7 times lower than that in Wistar rats, but the protein content of iNOS in 3-month-old OXYS rats (ELISA data) was increased. Perhaps such a paradoxical situation reflects a decreased reactivity of the immune system in the OXYS rats.

Publication types

  • English Abstract

MeSH terms

  • Age Factors
  • Aging / metabolism
  • Animals
  • Gene Expression Profiling
  • Humans
  • Macular Degeneration / metabolism*
  • Nitric Oxide Synthase Type I / genetics*
  • Nitric Oxide Synthase Type II / genetics*
  • Nitric Oxide Synthase Type III / genetics*
  • Rats
  • Retina / metabolism*
  • Statistics as Topic

Substances

  • Nitric Oxide Synthase Type I
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III