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Drug Metabolism and Disposition Fast Forward
First published on February 26, 2007; DOI: 10.1124/dmd.106.014282


0090-9556/07/3506-987-994$20.00
DMD 35:987-994, 2007

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Cyp1b1 Protein in the Mouse Eye during Development: An Immunohistochemical Study

Dharamainder Choudhary, Ingela Jansson, Karim Rezaul, David K. M. Han, Mansoor Sarfarazi, and John B. Schenkman

Departments of Pharmacology (D.C., I.J., J.B.S.), Surgery (D.C., M.S.), and Cell Biology (K.R., D.K.M.H.), University of Connecticut Health Center, Farmington, Connecticut

We show, for the first time, the spatiotemporal appearance of Cyp1b1 protein during mouse eye ontogeny. The protein was unambiguously identified in the adult mouse eye and newborn (P0) whole mouse microsomes and was shown to be localized in inner ciliary epithelium, corneal epithelium, retinal inner nuclear cells, and ganglion cells. The enzyme protein was present in the lens epithelium adjacent to the developing ciliary body at 15.5 days postconception (E15.5) and was most strongly expressed during E17.5 to 7 days postnatally (P07). Subsequently, it declined to very low levels. The protein was also expressed in the corneal endothelial cells adjacent to the ciliary body at P07. Cyp1b1 was barely detectable in the inner ciliary epithelium before E17.5 but increased rapidly postnatally, reaching adult levels by P28. Levels of the enzyme protein in the corneal epithelium were seen from E15.5 onward, increasing sharply, and after a decrease at P07, were highest in the adult animal eye. The presence of Cyp1b1 protein in the inner nuclear layer of the retina was very low in the prenatal eye, increasing rapidly postnatally, and was highest in the adult animal eye. In the ganglion cell layer of the retina, it increased slowly from E15.5 to P07 and then rapidly reached adult levels. Interestingly, Cyp1b1 was not detected in the trabecular meshwork at any stage of development or in the adult eye. We conclude that the enzyme may play important roles in normal eye development and function in mice as in humans, and that the mouse may prove to be an excellent model for determination of the roles of CYP1B1 in human eye development and function.


Address correspondence to: John B. Schenkman, Department of Pharmacology, University of Connecticut Health Center, Farmington, CT 06073. E-mail: jschenkm{at}neuron.uchc.edu







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