May 2004
Volume 45, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2004
Oxygen–induced retinopathy causes major changes in gene expression in younger mice, which correlates with a greater risk for neovascular response in younger versus older mice.
Author Affiliations & Notes
  • J.D. Ash
    Ophthalmology,
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
  • M. Balkis
    Ophthalmology,
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
  • H. Haniu
    Biochemistry,
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
  • H. Matsumoto
    Biochemistry,
    Univ of Oklahoma Hlth Sci Ctr, Oklahoma City, OK
  • Y. Tang
    Oklahoma Medicalical Research Foundation, Oklahoma City, OK
  • I. Dozmorov
    Oklahoma Medicalical Research Foundation, Oklahoma City, OK
  • M. Centola
    Oklahoma Medicalical Research Foundation, Oklahoma City, OK
  • Footnotes
    Commercial Relationships  J.D. Ash, None; M. Balkis, None; H. Haniu, None; H. Matsumoto, None; Y. Tang, None; I. Dozmorov, None; M. Centola, None.
  • Footnotes
    Support  NIH RR17703, EY14206, EY012190, RPB, OCAST HR02–140
Investigative Ophthalmology & Visual Science May 2004, Vol.45, 4050. doi:
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      J.D. Ash, M. Balkis, H. Haniu, H. Matsumoto, Y. Tang, I. Dozmorov, M. Centola; Oxygen–induced retinopathy causes major changes in gene expression in younger mice, which correlates with a greater risk for neovascular response in younger versus older mice. . Invest. Ophthalmol. Vis. Sci. 2004;45(13):4050.

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

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Abstract

Abstract: : Purpose:Mice exposed to oxygen from postnatal day 7 to 13 develop a transient proliferative retinopathy that will spontaneously and rapidly resolve without causing any long–term disease. We have found that mice exposed to oxygen from postnatal day 2 to 9 develop a more severe disease with long–term complications. The data suggest that older rodents have an endogenous mechanism of self–repair and protection from proliferative retinopathy. Our goal is determine the molecular mechanisms for the self–protection in older mice which is deficient in younger mice. Methods:We exposed mice to 75% oxygen at two different ages, P7 to P13 and P2 to P9. We collected eyes from mice at various time points following return to room air. We then dissected retinas and isolated RNA and proteins for use in DNA microarray and proteomic analysis respectively. Results:We have observed that younger retinas have a very different gene expression response to oxygen than older mice. At the RNA level there were 75 genes that had similar oxygen regulation, independent of age. However, there were more than 2000 genes that were regulated in one age but not the other. There were major differences at the protein level as well. In our screens we have identified several genes that have a know role in vascular development and stabilization. Conclusions:Like humans, the age of oxygen exposure is an important determinant for disease severity and the risk of long–term complications in mice. We are now using the younger–exposed model to determine the molecular cause for this increased risk at younger ages and the mechanism of self protection at older ages. We have found that younger retinas have a distinct molecular response to the oxygen insult and subsequent neovascularization than older retinas. We are currently analyzing candidate genes to determine which are involved in increased neovascular disease or self–protection.

Keywords: gene microarray • proteomics • retinopathy of prematurity 
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