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J. Biol. Chem., Vol. 277, Issue 33, 30191-30197, August 16, 2002

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Muscle Expression of Human Retinol-binding Protein (RBP)
SUPPRESSION OF THE VISUAL DEFECT OF RBP KNOCKOUT MICE^*

Loredana Quadro^§, William S. Blaner^¶, Leora Hamberger^¶, Russell N. Van Gelder^**, Silke Vogel^¶, Roseann Piantedosi^¶, Peter Gouras, Vittorio Colantuoni^§, and Max E. Gottesman

From the  Institute of Cancer Research and the Departments of ^¶ Medicine and  Ophthalmology, Columbia University, College of Physicians and Surgeons, New York, New York 10032, the ^§ Faculty of Biological Sciences, University of Sannio, 82100 Benevento, Italy, and the ^** Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63110

Mice lacking retinol-binding protein (RBP) have low circulating retinol levels. They have severe visual defects due to a low content of retinol or retinyl esters in the eye. A transgenic mouse strain that expresses human RBP under the control of the muscle creatine kinase promoter in the null background was generated. The exogenous protein bound retinol and transthyretin in the circulation and effectively delivered retinol to the eye. Thus, RBP expressed from an ectopic source suppresses the visual phenotype, and retinoids accumulate in the eye. No human RBP was found in the retinal pigment epithelium of the transgenic mice, indicating that retinol uptake by the eye does not entail endocytosis of the carrier RBP.

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