MyVisionTest News Archive
Dec 14, 2009
Microplasmin degrades fibronectin and laminin
Intravitreal microplasmin degrades fibronectin and laminin, two major extracellular matrix glycoproteins, at the vitreoretinal junction as well as at the outer retina, according to a new study performed on laboratory rats.
Vitreoretinal interaction has been implicated as possibly contributing to the onset of macular degeneration. Furthermore, traction at the vitreomacular interface is a major contributor to macular dysfunction, such as macular hole and cystoid macular edema. Vitreous detachment from the retina can occur spontaneously, or be surgically induced. However, surgery can lead to localized maculopathy, whereas incomplete vitreous separation can cause disease progression. An enzyme that could facilitate peeling of the posterior hyaloid would help to minimize surgically induced trauma and would provide a more uniform retinal surface.
Microplasmin (ThromboGenics) is a vitreolytic enzyme which is currently in Phase III clinical trials for the treatment of vitreomacular adhesion. An intravitreal injection of microplasmin may aid in releasing the posterior vitreous from the retinal surface and may yield complete posterior vitreous detachment (PVD) in some patients.
In the current study increasing doses of microplasmin were injected into the left eyes of 60 Sprague-Dawley rats to induce PVD. The right eyes were injected with the same volume of balanced salt solution (BSS). Histochemistry, scanning electron microscopy (SEM), and phase contrast microscopy were performed after 1 day and 7 days, to assess the remnant vitreous cortex. The fibronectin and laminin level located at the vitreoretinal interface and the outer retina were detected by immunohistochemistry.
Microplasmin induced complete PVD in a dose-dependent fashion, without internal limiting membrane (ILM) damage (P = 0.0001). The fibronectin and laminin in the photoreceptor cell layer (PCL) were completely degraded in all microplasmin-treated eyes. In eyes with complete PVD, the fibronectin, but not the laminin, was completely removed from the ILM by microplasmin treatment.
The investigators conclude that intravitreal injection of microplasmin degraded fibronectin and laminin at the vitreoretinal junction as well as at the outer retina.
Read more...
Curr Eye Res. 2009 Dec;34(12):1057-64
Tags: vitreous, microplasmin, animal study
Intravitreal microplasmin degrades fibronectin and laminin, two major extracellular matrix glycoproteins, at the vitreoretinal junction as well as at the outer retina, according to a new study performed on laboratory rats.Vitreoretinal interaction has been implicated as possibly contributing to the onset of macular degeneration. Furthermore, traction at the vitreomacular interface is a major contributor to macular dysfunction, such as macular hole and cystoid macular edema. Vitreous detachment from the retina can occur spontaneously, or be surgically induced. However, surgery can lead to localized maculopathy, whereas incomplete vitreous separation can cause disease progression. An enzyme that could facilitate peeling of the posterior hyaloid would help to minimize surgically induced trauma and would provide a more uniform retinal surface.
In the current study increasing doses of microplasmin were injected into the left eyes of 60 Sprague-Dawley rats to induce PVD. The right eyes were injected with the same volume of balanced salt solution (BSS). Histochemistry, scanning electron microscopy (SEM), and phase contrast microscopy were performed after 1 day and 7 days, to assess the remnant vitreous cortex. The fibronectin and laminin level located at the vitreoretinal interface and the outer retina were detected by immunohistochemistry.
Microplasmin induced complete PVD in a dose-dependent fashion, without internal limiting membrane (ILM) damage (P = 0.0001). The fibronectin and laminin in the photoreceptor cell layer (PCL) were completely degraded in all microplasmin-treated eyes. In eyes with complete PVD, the fibronectin, but not the laminin, was completely removed from the ILM by microplasmin treatment. The investigators conclude that intravitreal injection of microplasmin degraded fibronectin and laminin at the vitreoretinal junction as well as at the outer retina.
Read more...
Curr Eye Res. 2009 Dec;34(12):1057-64
