April 2014
Volume 55, Issue 13
Free
ARVO Annual Meeting Abstract  |   April 2014
Suppressing Thyroid Hormone Signaling Preserves Cone Photoreceptors in Mouse Models of Retinal Degeneration
Author Affiliations & Notes
  • Xi-Qin Ding
    Cell Biology, Univ Oklahoma Hlth Sciences Ctr, Oklahoma City, OK
  • Hongwei Ma
    Cell Biology, Univ Oklahoma Hlth Sciences Ctr, Oklahoma City, OK
  • Arjun Thapa
    Cell Biology, Univ Oklahoma Hlth Sciences Ctr, Oklahoma City, OK
  • Lynsie Morris
    Cell Biology, Univ Oklahoma Hlth Sciences Ctr, Oklahoma City, OK
  • T Michael Redmond
    The Laboratory of Retinal Cell and Molecular Biology, National Eye Institute, Bethesda, MD
  • Wolfgang Baehr
    John A. Moran Eye Center, University of Utah, Salt Lake City, UT
  • Footnotes
    Commercial Relationships Xi-Qin Ding, None; Hongwei Ma, None; Arjun Thapa, None; Lynsie Morris, None; T Redmond, None; Wolfgang Baehr, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science April 2014, Vol.55, 1713. doi:
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      Xi-Qin Ding, Hongwei Ma, Arjun Thapa, Lynsie Morris, T Michael Redmond, Wolfgang Baehr; Suppressing Thyroid Hormone Signaling Preserves Cone Photoreceptors in Mouse Models of Retinal Degeneration. Invest. Ophthalmol. Vis. Sci. 2014;55(13):1713.

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

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Abstract

Purpose: Cone phototransduction and survival of cones in the human macula is essential for color vision and for visual acuity. Progressive cone degeneration in age-related macular degeneration, Stargardt disease, and recessive cone dystrophies is a major cause of blindness. Thyroid hormone (TH) signaling which regulates cell proliferation, differentiation, and apoptosis plays a central role in cone opsin expression and patterning in the retina. Here, we investigated whether TH signaling affects cone viability in inherited retinal degeneration mouse models.

Methods: Rpe65-/- mice (a model of severe Leber congenital amaurosis or LCA) and Cpfl1 mice (severe recessive achromatopsia) were used to determine whether suppressing TH signaling (with anti-thyroid treatment) reduces cone death. Further, Cngb3-/- mice (moderate achromatopsia) and Gucy2e-/- mice (moderate LCA) were used to determine whether stimulating TH signaling (with triiodothyronine (T3) treatment) deteriorates cones. The serum T3 levels were analyzed by ELISA. Cone and rod survival were evaluated by examining cone density and expression levels of cone specific proteins using immunohistochemical and biochemical approaches, and by examining morphological integrity of the retinas.

Results: Cone density increased about 6-fold in Rpe65-/- and cpfl1 mice following anti-thyroid treatment and decreased about 40% in Cngb3-/- and Gucy2e-/- mice following T3 treatment. Anti-thyroid treatment did not affect rod survival, manifested as unchanged outer nuclear layer (ONL) thickness and the number of nuclei in ONL. However, T3 treatment significantly reduced ONL thickness and the number of nuclei in ONL in Cngb3-/- and Gucy2e-/- mice.

Conclusions: With multiple retinal degeneration mouse models, we demonstrate that TH signaling regulates photoreceptor viability in degenerating retinas. Suppressing TH signaling protects cones whereas stimulating TH signaling has a negative effect on both cones and rods. The findings of this study provide new insights into cone preservation and therapeutic interventions.

Keywords: 648 photoreceptors • 494 degenerations/dystrophies • 695 retinal degenerations: cell biology  
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