title: Retinol dehydrogenase 13 protects the mouse retina from acute light damage.
abstract: OBJECTIVE
  To investigate whether retinol dehydrogenase 13 (RDH13) can protect the retina from acute light-induced damage.
  
  
  METHODS
  We generated Rdh13 knockout mice using molecular biologic methods and assessed the associated morphological and functional changes under room-light conditions by hematoxylin-eosin (H&E), transmission electron microscopy (TEM), and scotopic electroretinography. Then, the light-damage model was established by exposure to diffuse white light (3,000 lx) for 48 h. Twenty-four h after light exposure, H&E was used for the histological evaluation. The thickness of the outer-plus-inner-segment and the outer nuclear layer was measured on sections parallel to the vertical meridian of the eye. An electroretinography test was performed to assess the functional change. Furthermore, the impairment of mitochondria was detected by TEM. Finally, the expression of cytochrome c (CytC) and other apoptosis-related proteins was detected by western blot.
  
  
  RESULTS
  We found that there was no obvious difference in phenotype or function between Rdh13 knockout and wild-type mice. In Rdh13(-/-) mice subjected to intense light exposure, the photoreceptor outer-plus-inner-segment and outer nuclear layer were dramatically shorter, and the amplitudes of a- and b-waves under scotopic conditions were significantly attenuated. Distinctly swollen mitochondria with disrupted cristae were observed in the photoreceptor inner segments of Rdh13(-/-) mice. Increased expression levels of CytC, CytC-responsive apoptosis proteinase activating factor-1 (Apaf-1) and caspases 3, and other mitochondria apoptosis-related genes (nuclear factor-kappa B P65 [P65] and B-cell lymphoma 2-associated X protein [Bax]) were observed in Rdh13(-/-) mice.
  
  
  CONCLUSIONS
  Rdh13 can protect the retina against acute light-induced retinopathy. The mechanism may involve inhibition of the mitochondrial apoptosis pathway.
authors.forename: Haiyan
authors.initials: H
authors.lastname: Wang
authors.forename: Xiaofang
authors.initials: X
authors.lastname: Cui
authors.forename: Qing
authors.initials: Q
authors.lastname: Gu
authors.forename: Yan
authors.initials: Y
authors.lastname: Chen
authors.forename: Jia
authors.initials: J
authors.lastname: Zhou
authors.forename: Ying
authors.initials: Y
authors.lastname: Kuang
authors.forename: Zhugang
authors.initials: Z
authors.lastname: Wang
authors.forename: Xun
authors.initials: X
authors.lastname: Xu
mesh_terms: D000429:Alcohol Oxidoreductases / Q000172:deficiency* / Q000235:genetics; D000818:Animals; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D045304:Cytochromes c / Q000235:genetics / Q000378:metabolism; D004596:Electroretinography; D015870:Gene Expression / Q000528:radiation effects; D008027:Light / Q000009:adverse effects; D051379:Mice; D018345:Mice, Knockout; D046529:Microscopy, Electron, Transmission; D008928:Mitochondria / Q000378:metabolism / Q000528:radiation effects; D016328:NF-kappa B / Q000235:genetics / Q000378:metabolism; D010786:Photoreceptor Cells / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D011833:Radiation Injuries, Experimental / Q000201:enzymology* / Q000209:etiology / Q000235:genetics; D012160:Retina / Q000378:metabolism* / Q000473:pathology / Q000528:radiation effects; D015398:Signal Transduction / Q000528:radiation effects; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D016328:NF-kappa B; D051028:bcl-2-Associated X Protein; D045304:Cytochromes c; D000429:Alcohol Oxidoreductases; C505409:Casp3 protein, mouse; D053148:Caspase 3