May 2005
Volume 46, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2005
Expression Profiles of Stress Related Genes During Light–Induced Retinal Damage in Rats
Author Affiliations & Notes
  • M. Chrenek
    Ophthalmology, Emory University, Atlanta, GA
  • M.L. Patterson
    Biological Sciences, University of Alberta, Edmonton, AB, Canada
  • R.M. Darrow
    Biochemistry/Molecular Biology, Wright State University School of Medicine, Dayton, OH
  • D.T. Organisciak
    Biochemistry/Molecular Biology, Wright State University School of Medicine, Dayton, OH
  • P. Wong
    Ophthalmology, Emory University, Atlanta, GA
  • Footnotes
    Commercial Relationships  M. Chrenek, None; M.L. Patterson, None; R.M. Darrow, None; D.T. Organisciak, None; P. Wong, None.
  • Footnotes
    Support  NSERC Operating (PW), NIH EY–01959 (DTO)
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1605. doi:
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      M. Chrenek, M.L. Patterson, R.M. Darrow, D.T. Organisciak, P. Wong; Expression Profiles of Stress Related Genes During Light–Induced Retinal Damage in Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1605.

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

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Abstract

Abstract: : Purpose: Light–induced retinal damage in rats is an animal model for analyzing molecular mechanisms involved in retinal degenerations. We have used this model system to identify genes that are differentially expressed during light damage. These results profile the changes in expression of 207 stress related genes during the time course of light damage and are useful in establishing the molecular profile of stress in this model system. Methods: Dark–reared Sprague–Dawley rats are treated with high intensity green light for 0, 8, 16, and 12/24 (12 hours light, 24 hours dark recovery). The animals are sacrificed and retinas dissected. Total RNA was extracted from the retinas and probed with Rat Stress Atlas Arrays (BD Sciences Clontech). Results: Of the 207 stress related genes on the array, 45 were of sufficient abundancy to be detected. 38/45 showed significant differences in abundance between the 4 time points studied. Groups of genes can be seen to have similar expression profiles with increases or decreases in expression with increasing light exposure. In addition, there are groups of genes that peak in expression at specific time points during light damage. The majority of heat shock genes increase in mRNA expression with light exposure. Interestingly, some of the crystallins (αA, ßB2 for example) follow the same trend as the heat shock proteins where as others do not (ßA1, ßA4, ßB1, ßB3). Conclusions: The grouping of stress related gene expression and differences in expression patterns of the groups indicates that the light–induced retinal damage is a dynamic process and likely involves more than one source of stress. This data also suggests that the expression of different crystallins in the retina respond to different induction signals and may reflect on differing functions for the crystallins. These results are important for establishing which molecular mechanisms are active at each time point and for the functional analysis of novel genes in further studies.

Keywords: stress response • gene screening • retina 
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