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Leandro B. Teixeira, Yun Zhao, Richard R. Dubielzig, Christine M. Sorenson, Nader Sheibani; Ultrastructural Abnormalities of the Trabecular Meshwork Associated with Cyp1b1-Deficiency. Invest. Ophthalmol. Vis. Sci. 2011;52(14):4632.
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To determine the ultra structural morphology of the iridocorneal drainage angle of Cyp1b1-deficient (Cyp1b1 -/-) mice.
Eyes from wild type (Cyp1b1+/+) and Cyp1b1-/- mice were enucleated and the globes were fixed for at least 8 h in 2.5% glutaraldehyde and processed for transmission electron microscopy. The iridocorneal angle, trabecular meshwork, Schlemm’s canal and aqueous veins were analyzed using a Philips CM120 Transmission electron microscope. Images were captured in digital format.
The 7-month-old C57BL/6 Cyp1b1 -/- mice presented marked disruption of the anterior and posterior trabecular meshwork, characterized by multifocal atrophy of the trabecular beams with accentuation of the intertrabecular spaces. The collagen of the beam cores was markedly fragmented and irregularly distributed. In addition, multifocal accumulations of elastic tissue in a nodular fashion were observed throughout the trabecular meshwork. The numbers of endothelial cells covering the surface of the trabecular beams was markedly diminished in Cyp1b1 -/- mice compared to Cyp1b1 +/+ mice, and were deposited in a multifocally disrupted basement membrane. Severe atrophy of the trabecular meshwork, which was characterized by the presence of a singular trabecular beam extending from the anterior to mid-meshwork, was observed in 8.5-month-old Cyp1b1 -/- mice. These beams contacted a collapsed posterior meshwork, where two or three trabecular beams were tightly packed and presented fragmented collagen and elastic fibers that surrounded few typical endothelial cells. Schlemm’s canal and the aqueous veins presented no abnormalities with Cyp1b1-deficiency.
The Cyp1b1 -/- mice presented ocular drainage ultrastructural abnormalities at 7-months and became more severe with age. The different arrays of structural lesions observed here suggest an age related evolution of the iridocorneal anomalies in the absence of Cyp1b1. Thus, Cyp1b1 expression and/or activity make significant contribution to the integrity and function of the trabecular meshwork.
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