May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Electroretinographic Findings in Knockin Mice With Gain of Function and Loss of Function Erythropoietin Receptor Signaling
Author Affiliations & Notes
  • R. Ray
    Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas
  • D. Yoon
    Hematology, University of Utah, Salt Lake City, Utah
  • M. M. Abd-El-Barr
    Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas
  • J. T. Prchal
    Hematology, University of Utah, Salt Lake City, Utah
  • S. M. Wu
    Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas
  • E. Holz
    Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas
  • T. A. Albini
    Bascom Palmer Eye Institute, Miami, Florida
  • P. E. Carvounis
    Cullen Eye Institute, Department of Ophthalmology, Baylor College of Medicine, Houston, Texas
  • Footnotes
    Commercial Relationships  R. Ray, None; D. Yoon, None; M.M. Abd-El-Barr, None; J.T. Prchal, None; S.M. Wu, None; E. Holz, None; T.A. Albini, None; P.E. Carvounis, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 4943. doi:https://doi.org/
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      R. Ray, D. Yoon, M. M. Abd-El-Barr, J. T. Prchal, S. M. Wu, E. Holz, T. A. Albini, P. E. Carvounis; Electroretinographic Findings in Knockin Mice With Gain of Function and Loss of Function Erythropoietin Receptor Signaling. Invest. Ophthalmol. Vis. Sci. 2008;49(13):4943. doi: https://doi.org/.

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

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Abstract

Purpose: : A growing body of evidence suggests that erythropoietin (Epo) plays a role in angiogenesis and neuroprotection. To investigate the possible role of erythropoietin in the retina we performed electroretinography in transgenic mice with gain-of-function and loss-of-function erythropoietin receptors (EpoR).

Methods: : The animal models of increased and decreased Epo signaling were previously generated by homologous recombination in mouse embryonic stem cells. The murine EpoR gene was replaced with a gain-of-function mutant human EPOR (mthEPOR, from a patient with primary familial polycythemia) and with a loss-of-function wild-type human EPOR gene (wthEPOR) (PNAS, 98:986, 2001). 3 mthEPOR and 4 wthEPOR homozygotes underwent simultaneous bilateral dark-adapted electroretinography at 4 and 12 months of age.

Results: : At 4 months mthEPOR mice had a greater saturated a-wave amplitude compared to wthEPOR mice (510±31µV (mean±SEM) compared to 410±26µV, p=0.034), while the difference in maximum b-wave amplitude did not reach statistical significance (mthEPOR mice 490±38µV compared to wthEPOR 437±37µV). At 12 months mthEPOR mice had a statistically greater maximum b-wave amplitude compared to wthEPOR (400±8µV compared to 232±17µV, p=0.0006) mice while the difference in saturated a-wave amplitude failed to reach statistical significance (452±27µV compared to 367±21µV, p=0.21).

Conclusions: : The greater a- and b- wave amplitudes found in the gain-of-function EpoR signaling mice may indicate that erythropoietin is a neurotrophic factor in the neurosensory retina. Histological analyses may corroborate structural differences that account for our electroretinographic findings.

Keywords: neuroprotection • electroretinography: clinical • growth factors/growth factor receptors 
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