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Biology and Diseases of Rabbits

ABSTRACT: Beginning in 1931, an inbred rabbit colony was developed at the Phipps Institute for the Study, Treatment and Prevention of Tuberculosis at the University of Pennsylvania. This colony was used to study natural resistance to infection with tuberculosis (Robertson et al., 1966). Other inbred colonies or well-defined breeding colonies were also developed at the University of Illinois College of Medicine Center for Genetics, the Laboratories of the International Health Division of The Rockefeller Foundation, the University of Utrecht in the Netherlands, and Jackson Laboratories. These colonies were moved or closed in the years to follow. Since 1973, the U.S. Department of Agriculture has reported the total number of certain species of animals used by registered research facilities (1997). In 1973, 447,570 rabbits were used in research. There has been an overall decrease in numbers of rabbits used. This decreasing trend started in the mid-1990s. In 2010, 210,172 rabbits were used in research. Despite the overall drop in the number used in research, the rabbit is still a valuable model and tool for many disciplines.

SUBMITTER: Nowland M

PROVIDER: S-EPMC7150064 | biostudies-literature | 2015 Jan

REPOSITORIES: biostudies-literature

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Project description:PurposeTo evaluate wound healing in rabbit corneas that developed a spontaneous persistent epithelial defect (PED) after photorefractive keratectomy (PRK).MethodsForty-eight 10- to 15-week-old female New Zealand White rabbits weighing 2.5 to 3.0 kg underwent either -3 diopter (D) or -9 D PRK to generate a series of corneas to study wound healing after injury. During that series, seven corneas developed a PED detected with 1% fluorescein staining at a slit lamp that either did not have epithelial closure by 1 week after surgery or subsequently had the closed epithelium break down to form a PED 2 to 3 weeks after surgery. The corneas had slit-lamp photography, with and without 1% fluorescein, and were removed from the normal PRK series. Each PED cornea was evaluated using immunohistochemistry for the myofibroblast marker α-smooth muscle actin (α-SMA), keratocyte marker keratocan, and mesenchymal cell marker vimentin, as well as basement membrane components perlecan and collagen type IV.ResultsAll seven corneas that had PRK with a PED, even the two evaluated at only 1 week after PRK, had α-SMA-positive myofibroblasts populating the anterior stroma within the PED, along with comingled α-SMA-negative cells that were likely corneal fibroblasts and possibly bone marrow-derived fibrocytes. Both perlecan and collagen type IV accumulated in the anterior stroma of the epithelial defects without an epithelial basement membrane, likely produced by corneal fibroblasts to modulate transforming growth factor-β entering the stroma from the tears and peripheral epithelium.ConclusionsCorneas with a PED that occurred following PRK (a procedure that produces a transient neurotropic state in the cornea) had myofibroblasts populating the superficial stroma within the epithelial defect as early as 1 week after the surgery.Translational relevancePharmacologic treatments that trigger myofibroblast apoptosis, including topical losartan, could facilitate decreased scarring fibrosis in corneas with a PED.

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Biology and Diseases of Rabbits

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