April 2011
Volume 52, Issue 14
Free
ARVO Annual Meeting Abstract  |   April 2011
The Role Of Galectin-3 In Regulating The Neuroprotective Wnt Signaling Pathway: A Potential Link To AMD
Author Affiliations & Notes
  • Nikisha Kothari
    Ophthalmology, University of Miami Miller School of Medicine, Miami, Florida
  • Hyun Yi
    Ophthalmology, University of Miami Miller School of Medicine, Miami, Florida
  • Nora Caberoy
    Ophthalmology, University of Miami Miller School of Medicine, Miami, Florida
  • Wei Li
    Ophthalmology, University of Miami Miller School of Medicine, Miami, Florida
  • Abigail S. Hackam
    Ophthalmology, University of Miami Miller School of Medicine, Miami, Florida
  • Footnotes
    Commercial Relationships  Nikisha Kothari, None; Hyun Yi, None; Nora Caberoy, None; Wei Li, None; Abigail S. Hackam, None
  • Footnotes
    Support  Fight for Sight Inc., Karl Kirchgessner Foundation, NEI Core Grant, Research to Prevent Blindness Departmental Support
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 2670. doi:
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      Nikisha Kothari, Hyun Yi, Nora Caberoy, Wei Li, Abigail S. Hackam; The Role Of Galectin-3 In Regulating The Neuroprotective Wnt Signaling Pathway: A Potential Link To AMD. Invest. Ophthalmol. Vis. Sci. 2011;52(14):2670.

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Abstract

Purpose: : We previously demonstrated that the Wnt signaling pathway is activated in Muller glia during photoreceptor death and that Wnt activation protects photoreceptors from oxidative stress. The galectin-3 protein is a potential regulator of Wnt signaling because of its expression in age-related macular degeneration (AMD) retinas, its regulation of Wnt signaling in colon cancer, and its protection of photoreceptors from light damage. The relationship between Wnt signaling and galectin-3 has not been examined in the retina. In this study, we investigated galectin-3 regulation of Wnt signaling and the influence of galectin-3 on cell viability.

Methods: : The Muller glia cell line MIO-M1 and the retinal pigment epithelium cell line ARPE-19 were used. Cell lines were transfected with galectin-3 cDNA using lipofectamine and expression of galectin-3 protein was confirmed by Western blot. Activation of Wnt signaling was measured by Western blot and luciferase reporter assays with the TOP-FLASH and Renilla plasmids. ARPE-19 cells were injured using oxidative stress (0.4mM H2O2 for 24 hours) and co-treated with Wnt3a ligand to induce the Wnt pathway. Cell viability was measured by WST1 assay.

Results: : Endogenous galectin-3 is expressed in retinal pigment epithelial ARPE-19 and Muller glia MIO-M1 cells. Over-expression of galectin-3 increased Wnt signaling 1.9 fold in ARPE-19 cells, as measured by luciferase assay (n=4, p<0.05), and by 1.33 fold in MIO-M1 cells, as measured by Western blot (n=5, p<0.05). In the absence of oxidative damage, galectin-3 did not alter ARPE-19 viability. However, when ARPE-19 cells were injured by oxidative stress, galectin-3 increased viability by 40% (n=5, p<0.05), and by 24% when co-treated with Wnt3a-containing condition media (n=4, p<0.05).

Conclusions: : These results indicate that galectin-3 upregulates the Wnt pathway and increases viability of retinal pigment epithelial cells, suggesting galectin-3 and Wnt signaling may interact in the retina. This finding is potentially significant to the pathogenesis of AMD because galectin-3 is secreted from RPE cells during AMD injury.

Keywords: age-related macular degeneration • retinal degenerations: cell biology • apoptosis/cell death 
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