April 2010
Volume 51, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2010
Retinal Vascular Degeneration and Macroglia Changes in the Transgenic P23H Rat Model of Retinitis Pigmentosa
Author Affiliations & Notes
  • I. Pinilla
    Ophthalmology, Hospital Univ Miguel Servet, Zaragoza, Spain
    Instituto Aragones de Ciencias de la Salud, Zaragoza, Spain
  • L. Fernandez-Sanchez
    Fisiologia, Genetica y Microbiologia, Universidad de Alicante, Alicante, Spain
  • G. Esquiva
    Fisiologia, Genetica y Microbiologia, Universidad de Alicante, Alicante, Spain
  • N. Cuenca
    Fisiologia, Genetica y Microbiologia, Universidad de Alicante, Alicante, Spain
  • Footnotes
    Commercial Relationships  I. Pinilla, None; L. Fernandez-Sanchez, None; G. Esquiva, None; N. Cuenca, None.
  • Footnotes
    Support  MEC (BFU2006-00957/BFI, BFU2009-07793/BFI), FIS PS09/01854, MSyC RETICS RD07/0062/0012, FUNDALUCE, ONCE, and Fundación Médica Mutua Madrileña.
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4069. doi:
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      I. Pinilla, L. Fernandez-Sanchez, G. Esquiva, N. Cuenca; Retinal Vascular Degeneration and Macroglia Changes in the Transgenic P23H Rat Model of Retinitis Pigmentosa. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4069.

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Abstract

Purpose: : Retinitis pigmentosa and allied diseases affect the structure and function of photoreceptors. Secondarily to the loss of photoreceptors a reduction of retinal vascularization takes place, which seems to influence the cellular degenerative process. Retinal macroglial cells, astrocytes and Müller cells, provide support for retinal neurons and regulate retinal function, are important for energetic metabolism and are crucial for maintaining the blood retinal barrier. The aim of this study was to investigate the evolution of the retinal capillary plexus during retinal degeneration and their relationship with macroglia in the P23H rat.

Methods: : Homozygous P23H line-3 rats aged from 18 days to 16 months were used in this study, Sprague-Dawley (SD) rats were used as controls. The retinas were stained using NADPH diaphorase histochemistry on whole-mount preparations in order to visualize the retinal vascular-network. The vascular plexi of each retinas were drawn using a camera lucida. Glial cells were labelled using immunocytochemical procedures. Morphometrical analysis was carried out using the NIH ImageJ software.

Results: : In the 4 months old P23H retina a lower density of the capillary plexus could be observed with significant loss of retinal capillary loops. Regarding the intermediate plexus, it was virtually disappeared at this age, and the remaining two plexi appeared connected by perpendicular vessels. At 16 months the deep capillary plexus was completely lost, and only vessels exhibiting an abnormal, tortuous dead-end could be observed. The superficial vascular layer, formed by arteries and veins, at 4 months old was richer in the P23H rat comparing to SD, and experienced an increase in density thereafter until 12 months old. During retinal degeneration glial cells were activates with an increase of microglia, expression of GFAP in Müller cels and morphological changes in astrocytes, specially in sucker end-feet.

Conclusions: : In retinitis pigmentosa the loss of photoreceptors is accompanied by degenerative changes in the retinal vascular network. The disruption of capillary plexi with loss of capillary loops can affect the normal oxygen and nutrient supply to retinal cells, and thereby accelerate the progress of retinal degeneration. Vascular impairment is accompanying with changes in glial cells. Changes in retinal vascularization must be taken into account in the design of therapies targeting this disease.

Keywords: retinal degenerations: cell biology 
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