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2009 | 69 | 3 |

Tytuł artykułu

The neuroprotective effects of urocortin 2 in bilateral common carotid occlusion induced retinal degeneration

Warianty tytułu

Języki publikacji

EN

Abstrakty

EN
Urocortin 2 (Ucn 2) is a CRF paralog that preferentially activates CRF2 receptors. Little is known regarding potential retinoprotective effects of Ucns despite the known presence of CRF family peptides and their receptors in retina. We investigated the effects of intravitreal Ucn 2 administration on ischemia-induced retinal degeneration (BCCAO). Two-month-old rats were subjected to BCCAO and their retinas were processed histologically after two weeks survival to determine the density of viable cells in the ganglionic cell layer and the thickness of all retinal layers. Immunohistological analysis of PKC-, calretinin-immunoreactivity was also performed. In BCCAO reduced retina thickness by approximately 60% as compared to sham-operated animals. Intraocular Ucn 2 treatment led to a nearly intact appearance of the retinal layers, and the thickness of all layers was signifi cantly increased by 40% compared to ischemic vehicle-treated subjects. Ucn 2 treatment also increased the number of cells by 55% in the ganglionic cell layer as compared to those from carotid-occluded retinas of vehicle-treated subjects. Ucn 2 also reversed the alterations found in the pattern of immunocytochemical markers, such as calretinin and PKC. These fi ndings suggest that intraocular Ucn 2 treatment may protect against ischemia-induced retinal degeneration, results with potential therapeutic implications for ophthalmic diseases. Support: OTKA: K72592; F67830; 78480; T061766; Richter.

Słowa kluczowe

Wydawca

-

Rocznik

Tom

69

Numer

3

Opis fizyczny

p.310

Twórcy

autor
  • Department of Experimental Zoology and Neurobiology, University of Pecs, Pecs, Hungary
autor
  • Department of Sportbiology, University of Pecs, Pecs, Hungary
autor
  • Department of Anatomy, University of Pecs, Pecs, Hungary
autor
  • Department of Anatomy, University of Pecs, Pecs, Hungary
autor
  • Department of Experimental Zoology and Neurobiology, University of Pecs, Pecs, Hungary
autor
  • Department of Anatomy, University of Pecs, Pecs, Hungary
autor
  • Department of Anatomy, University of Pecs, Pecs, Hungary
autor
  • Department of Physiology, University of Pecs, Pecs, Hungary
autor
  • Department of Physiology, The Scripps Research, California, Florida, USA
autor
  • Department of Experimental Zoology and Neurobiology, University of Pecs, Pecs, Hungary

Bibliografia

Typ dokumentu

Bibliografia

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