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Vom Hagen, F., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany, V. Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer, 68167 Mannheim, Germany
Feng, Y., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Hillenbrand, A., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Hoffmann, S., Medical Research Center, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Shani, M., Institute of Animal Science, Volcani Center, Bet Dagan, Israel
Deutsch, U., Theodor Kocher Institute, University of Berne, Berne, Switzerland
Hammes, H.P., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Incipient diabetic retinopathy is characterized by increased capillary permeability and progressive capillary occlusion. The earliest structural change is the loss of pericytes (PC) from the retinal capillaries. With the availability of the XLacZ mouse, which expresses the LacZ reporter in a PC/vascular smooth muscle cell (vSMC) specific fashion, we quantitatively assessed the temporal dynamics of smooth muscle cells in arterioles under hyperglycemic conditions. We induced stable hyperglycemia in XLacZ mice. After 4, 8, and 12 weeks of diabetes retinae were isolated and β-galctosidase/ lectin stained. The numbers of smooth muscle cells were counted in retinal whole mounts, and diameters of retinal radial and branching arterioles and venules were analyzed at different distances apart from the center of the retina. After eight weeks of diabetes, the numbers of vSMCs were significantly reduced in radial arterioles 1000 μm distant from the optic disc. At proximal sites of branching arterioles (400 μm distant from the center), and at distal sites (1000 μm), vSMC were significantly reduced already after 4 weeks (to a maximum of 31%). These changes were not associated with any measurable variation in vessel diameters. These data indicate quantitatively that hyperglycemia not only causes pericyte loss, but also loss of vSMCs in the retinal vasculature. Our data suggest that arteriolar vSMC in the eye underlie similar regulations which induce early pericyte loss in the diabetic retina. © J. A. Barth Verlag in Georg Thieme Verlag KG.
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Early loss of arteriolar smooth muscle cells: More than just a pericyte loss in diabetic retinopathy
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Vom Hagen, F., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany, V. Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer, 68167 Mannheim, Germany
Feng, Y., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Hillenbrand, A., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Hoffmann, S., Medical Research Center, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Shani, M., Institute of Animal Science, Volcani Center, Bet Dagan, Israel
Deutsch, U., Theodor Kocher Institute, University of Berne, Berne, Switzerland
Hammes, H.P., 5Th Medical Clinic, Faculty of Medicine Mannheim, University of Heidelberg, Mannheim, Germany
Early loss of arteriolar smooth muscle cells: More than just a pericyte loss in diabetic retinopathy
Incipient diabetic retinopathy is characterized by increased capillary permeability and progressive capillary occlusion. The earliest structural change is the loss of pericytes (PC) from the retinal capillaries. With the availability of the XLacZ mouse, which expresses the LacZ reporter in a PC/vascular smooth muscle cell (vSMC) specific fashion, we quantitatively assessed the temporal dynamics of smooth muscle cells in arterioles under hyperglycemic conditions. We induced stable hyperglycemia in XLacZ mice. After 4, 8, and 12 weeks of diabetes retinae were isolated and β-galctosidase/ lectin stained. The numbers of smooth muscle cells were counted in retinal whole mounts, and diameters of retinal radial and branching arterioles and venules were analyzed at different distances apart from the center of the retina. After eight weeks of diabetes, the numbers of vSMCs were significantly reduced in radial arterioles 1000 μm distant from the optic disc. At proximal sites of branching arterioles (400 μm distant from the center), and at distal sites (1000 μm), vSMC were significantly reduced already after 4 weeks (to a maximum of 31%). These changes were not associated with any measurable variation in vessel diameters. These data indicate quantitatively that hyperglycemia not only causes pericyte loss, but also loss of vSMCs in the retinal vasculature. Our data suggest that arteriolar vSMC in the eye underlie similar regulations which induce early pericyte loss in the diabetic retina. © J. A. Barth Verlag in Georg Thieme Verlag KG.
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