May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Inherited Photoreceptor Degeneration Is Delayed and Vision Preserved by Over Expression of Thioredoxin in the Tubby Mouse
Author Affiliations & Notes
  • J. F. McGinnis
    Oklahoma University Hlth Sci Ctr, Oklahoma City, Oklahoma
    Cell Biology / Ophthalmology; Oklahoma Center for Neuroscience,
  • X. Zhou
    Oklahoma University Hlth Sci Ctr, Oklahoma City, Oklahoma
    Ophthalmology,
  • L. Kong
    Oklahoma University Hlth Sci Ctr, Oklahoma City, Oklahoma
    Ophthalmology,
  • F. Li
    Oklahoma University Hlth Sci Ctr, Oklahoma City, Oklahoma
    Ophthalmology,
  • J. Yodoi
    Department of Biological Responses, Kyoto University Japan., Kyoto 606-8507, Japan
  • W. Cao
    Oklahoma University Hlth Sci Ctr, Oklahoma City, Oklahoma
    Ophthalmology,
  • Footnotes
    Commercial Relationships  J.F. McGinnis, None; X. Zhou, None; L. Kong, None; F. Li, None; J. Yodoi, None; W. Cao, None.
  • Footnotes
    Support  NIH NCRR (P20-RR017703); Oklahoma Center for Advancement of Science and Technology, Foundation Fighting Blindness, Research to Prevent Blindness
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4930. doi:https://doi.org/
  • Views
  • Share
  • Tools
    • Alerts
      ×
      This feature is available to authenticated users only.
      Sign In or Create an Account ×
    • Get Citation

      J. F. McGinnis, X. Zhou, L. Kong, F. Li, J. Yodoi, W. Cao; Inherited Photoreceptor Degeneration Is Delayed and Vision Preserved by Over Expression of Thioredoxin in the Tubby Mouse. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4930. doi: https://doi.org/.

      Download citation file:


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

      ×
  • Supplements
Abstract

Purpose: : Thioredoxin (Trx) has neurotrophic factor-like activity and may play a crucial role in maintaining neuronal cell integrity. In this study, the neuroprotective effect of Trx on photoreceptor degeneration in tubby (tub) mouse, a phenotypical model of sensorineural deafness/retinal dystrophic syndromes, was examined.

Methods: : Human-Trx transgenic (Tg-Trx) mice were crossed with homozygous tubby mice. Protective effects of the over expression of Trx were evaluated morphologically by quantitative histology and functionally by electroretinography (ERG). Immunohistochemistry was performed to localize the expression of Trx in the retina. Real-Time qPCR, RT-PCR and Western blot analysis were used to examine the expression of the Trx mRNA and its protein. In addition, the levels of selected neuroprotective proteins and their mRNAs were evaluated in the retinas of control and experimental mice.

Results: : Our data clearly demonstrate a significant overexpression of the mRNA for Trx and its protein in the retinas of Tg-Trx/tub mice compared to that of tubby mice. At P34, the amplitude of the ERG b-wave and the outer nuclear layer thickness were significantly increased in Tg-Trx/tub mice (p<0.01). Overexpression of Trx extensively up-regulated retinal levels of brain-derived neurotrophic factor (BDNF), glial-derived neurotrophic factor (GDNF) and fibroblast growth factor-basic (FGF-b) in Tg-Trx/tub mice, reaching levels observed in wild type mice.

Conclusions: : Trx strongly delays photoreceptor degeneration and preserves visual function in tubby mice. BDNF, GDNF and FGF-b may be involved in the mechanism of Trx-mediated photoreceptor protection in this model.

Keywords: neuroprotection • retinal degenerations: cell biology • transgenics/knock-outs 
×
×

This PDF is available to Subscribers Only

Sign in or purchase a subscription to access this content. ×

You must be signed into an individual account to use this feature.

×