Ultrastructural abnormalities of the trabecular meshwork extracellular matrix in Cyp1b1-deficient mice.

Publications // Richard Dubielzig // Sheibani Lab // Mar 01 2015

PubMed ID: 24879660

Author(s): Teixeira LB, Zhao Y, Dubielzig RR, Sorenson CM, Sheibani N. Ultrastructural abnormalities of the trabecular meshwork extracellular matrix in Cyp1b1-deficient mice. Vet Pathol. 2015 Mar;52(2):397-403. doi: 10.1177/0300985814535613. Epub 2014 May 30. PMID 24879660

Journal: Veterinary Pathology, Volume 52, Issue 2, Mar 2015

Cytochrome P450 1B1 (CYP1B1) is highly expressed in human and murine ocular tissues during development. Mutations in this gene are implicated in the development of primary congenital glaucoma (PCG) in humans. Mice deficient in Cyp1b1 (Cyp1b1(-/-) ) present developmental abnormalities similar to human primary congenital glaucoma. The present work describes the ultrastructural morphology of the iridocorneal angle of 21 eyes from 1-week-old to 8-month-old Cyp1b1(-/-) mice. Morphometric and semiquantitative analysis of the data revealed that 3-week-old Cyp1b1(-/-) mice present a significantly (P < .005) decreased amount of trabecular meshwork (TM) collagen and higher TM endothelial cell and collagen lesion scores (P < .005) than age-matched controls. Collagen loss and lesion scores were progressively increased in older animals, with 8-month-old animals presenting severe atrophy of the TM. Our findings advance the understanding of the effects of CYP1B1 mutations in TM development and primary congenital glaucoma, as well as suggest a link between TM morphologic alterations and increased intraocular pressure.

© The Author(s) 2014.