June 2015
Volume 56, Issue 7
Free
ARVO Annual Meeting Abstract  |   June 2015
Increased retinaldehyde dehydrogenase activity during recovery from induced myopia
Author Affiliations & Notes
  • Angelica Harper
    Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK
  • Gennadiy P Moiseyev
    Physiology, University of Oklahoma Health Sciences Center, Oklahoma City, OK
  • Jody Ann Summers
    Cell Biology, University of Oklahoma Health Sciences Center, Oklahoma City, OK
  • Footnotes
    Commercial Relationships Angelica Harper, None; Gennadiy Moiseyev, None; Jody Summers, None
  • Footnotes
    Support None
Investigative Ophthalmology & Visual Science June 2015, Vol.56, 5845. doi:
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      Angelica Harper, Gennadiy P Moiseyev, Jody Ann Summers; Increased retinaldehyde dehydrogenase activity during recovery from induced myopia. Invest. Ophthalmol. Vis. Sci. 2015;56(7 ):5845.

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

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Abstract

Purpose: Previous studies have identified significant increases in retinaldehyde dehydrogenase 2 (RALDH2) steady state mRNA in the chick choroid during recovery from myopic defocus. Thus, RALDH2 may be responsible for the increase in choroidal all-trans-retinoic acid (atRA) synthesis observed during recovery from myopic defocus. The present study examines RALDH activity and RALDH2 protein expression in control and recovering chick ocular tissues to further elucidate the link between RALDH2, atRA, and visually guided ocular growth.

Methods: Myopia was induced in chicks by form deprivation for 10 days, followed by up to 15 days of recovery. Retina/RPE, choroid, and/or sclera were isolated from control (not treated) and recovering (treated) eyes at various points during recovery. RALDH catalytic activity was measured in tissue homogenates using an in vitro atRA synthesis assay together with HPLC quantification of synthesized atRA. RALDH2 protein expression in control and recovering homogenates was compared by western blotting.

Results: RALDH activity was increased in recovering choroids as compared to controls by 66.5% (p > 0.01, paired t-test) at day 3 of recovery and by 49.7% (p > 0.05, paired t-test) at day 7 (n = 6). When RALDH activity in control and day 4 recovering retina/RPE, choroid, and sclera was compared, RALDH activity could only be detected in the choroid (n = 9). Western blot analyses indicated that RALDH2 protein expression was highest in the choroid and minimal in retina/RPE and sclera. Choroidal RALDH2 expression was 281.1% greater (p > 0.05, paired t-test) in recovering eyes as compared with controls (n = 3). <br /> <br />

Conclusions: These results demonstrate that the choroid is the major ocular tissue exhibiting RALDH activity, which is responsible for increased RALDH activity during recovery. These increases correspond to increases in choroidal RALDH2 protein expression, suggesting that increased RALDH activity in the recovering choroid is due to increased RALDH2 protein expression. These results suggest that RALDH2 may be useful as a therapeutic target for the treatment of myopia.

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