May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Expression of TNF-and TNF-R1 of Retinal Glial Cells in Rat Chronic Elevated Intraocular Pressure Model
Author Affiliations & Notes
  • X.-H. Sun
    Ophthalmology, Fudan Univ of EYE & ENT Hospital, Shanghai, China
  • Z. Ling
    Ophthalmology, Fudan Univ of EYE & ENT Hospital, Shanghai, China
  • Footnotes
    Commercial Relationships  X. Sun, None; Z. Ling, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 5485. doi:https://doi.org/
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      X.-H. Sun, Z. Ling; Expression of TNF-and TNF-R1 of Retinal Glial Cells in Rat Chronic Elevated Intraocular Pressure Model. Invest. Ophthalmol. Vis. Sci. 2008;49(13):5485. doi: https://doi.org/.

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

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Abstract

Purpose: : In order to study the effects of retinal glial cell on glaucomatous retinal ganglion cells damage, Expression of TNF-αand TNF-R1 of retinal glial cells was observed in rat model with chronic elevated intraocular pressure glaucoma

Methods: : 1.Rats were rendered elevated intraocular pressure by ligating 2 episcleral veins with subconjunctival injection 5-Fu. 2.Four weeks after operation, immuno-histological assays were carried out on cryostat sections. The co-expression of TNF-α-GFAP, TNF-α-OX42 , TNFR-1-GFAP ,and TNFR-1-NeuN were observed via a confocal laser scanning microscope , respectively.

Results: : 1. In the normal and sham-operated control eyes, the average IOP was 12.45 mmHg and 14.84 mmHg respectively. After operation, the mean IOP of the experimental eyes immediately increased to 39.26 mmHg, and it remained significantly elevated for the entire length of the experiment. The ocular tissues including cornea, lens and sclera appeared normal throughout the experiment.2. By immunohistochemistry, no ( or very faint if any ) staining for TNF-α is present in retina from normal rats. TNF-α is not present in GFAP-position astrocytes, Müller cells, or in OX42-position microglia. In glaucomatous retina, many areas of focal staining for TNF-α are apparent. The intensity of the immunostaining and the number of stained cells for TNF- were notably greater than that in normal eyes. TNF- α position immunoreactivity is mainly present in retinal ganglion cell and nerve fiber layers, as well as in inner nuclear layer, and is co-localized to GFAP-positive astrocytes, Müller cells ,and in OX42 -positive microglial in glaucoma. By immunohistochemistry, no ( or very faint if any ) staining for TNFR-1 is present in retina from normal rats. In glaucomatous eyes, the intensity of the immunostaining and the number of stained cells for TNFR-1 were notably greater than that in normal eyes. Positive immunostaining for TNFR-1 in retinal sections from glaucomatous eyes was limited to the nerve fiber and retinal ganglion cell layers, mostly co-localized with GFAP in astrocytes, but no neuron cells in the nerve fiber and retinal ganglion cell layers are positive for TNFR-1.

Conclusions: : TNF-α that actived retinal glial cells secrete may play an important role in glaucomatous retinal ganglion cell damage.

Keywords: retinal glia • ganglion cells • neuro-ophthalmology: optic nerve 
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