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E. Fahl, N. Tanimoto, S. C. Beck, V. Oberhauser, S. Hessel, N. B. Ghyselinck, A. Wyss, J. von Lintig, M. W. Seeliger; Functional Consequences of Retinoid Depletion in Mice. Invest. Ophthalmol. Vis. Sci. 2007;48(13):2996.
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To investigate the functional impact of retinoid depletion in RBP4-/-BCMO1-/- double knock-out mice.
RBP4-/-BCMO1-/- double knock-out mice were generated by crossing retinol binding protein knock-out mice (RBP4-/-) representing systemic retinol deficiency and ß-carotene 15,15’-monooxygenase knock-out mice (BCMO1-/-) lacking the ß-carotene cleavage enzyme. Retinal function of dark-adapted mice aged 3 months was analyzed with both scotopic and photopic single flash and flicker electroretinography (ERG). Morphology was examined in vivo with scanning-laser-ophthalmology (SLO). Whole eye retinoid content was determined by HPLC. The study was performed in accordance with the ARVO Statement for the Use of Animals in Ophthalmic and Vision Research.
RBP4-/-BCMO1-/- double knock-out mice showed a much stronger reduction in ocular retinoid levels than the RBP4-/- knock-out mice. HPLC analysis of the whole eye extracts revealed no detectable retinyl esters and only trace amounts of 11-cis-retinal. Functionally, these mice showed a pathological right shift both in the VlogI function of scotopic single flash recordings and the amplitude peak of the 6Hz flicker ERG. In SLO imaging, severe morphological changes, including persistent vitreal vessels and colobomas, were observed.
The lack of both the retinol-binding-protein and the ß-carotene cleavage enzyme in RBP4-/-BCMO1-/- double knock-out mice led to a severe retinoid-deficiency of the eyes that caused severe functional and structural alterations.
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