Abstract
Abstract: :
Purpose: In the course of proliferative retinopathies, cells in the neovascular membrane can generate force causing tractional retinal detachment. The source of the contractile cells and the mechanism causing their development are not well understood. Recently, two different transgenic mouse models have been generated that have severe tractional retinal detachment. The purpose of this study was to identify contractile cells in the vitreous and retinas of these mouse models and to determine their origin and pattern of growth. Methods: We have isolated retinas at various developmental ages from transgenic mice expressing leukemia inhibitory factor in the lens (LIF), or platelet-derived growth factor B (PDGFB) in the retina. The whole retinas were stained for smooth muscle α actin (SMA) to identify contractile myofibroblasts. Retinas at different ages were compared to identify the developmental source of contractile cells. Results: In the LIF transgenic mice, we have observed the accumulation of neovascular membranes in the vitreous, which results in tractional retinal detachment by four weeks of age. In two to three week old mice, SMA positive myofibroblasts that are organized into planar sheets of cells capable of generating tractional force along the axis of the vascularized membranes. In the PDGFB mice, we have observed the accumulation of SMA positive cells that have the morphological appearance of myofibroblasts located within the retina. The cells are organized into a loose network with their actin filaments oriented so that the sum of their force generation is parallel to the inner limiting membrane. Conclusions: Both transgenic models have tractional retinal detachment. In the LIF mice, the force is generated in the vitreous, while in the PDGFB mice, the force is generated in the retinas itself. The developmental studies suggest that the myofibroblasts may be derived from vascular smooth muscle cells.
Keywords: retinal detachment • animal model • proliferative vitreoretinopathy