Increased basement membrane thickness, pericyte ghosts, and loss of retinal thickness and cells in dopamine beta hydroxylase knockout mice
| Autor: | Steven A. Thomas, Christopher P. Smith, Lisa S. McFadyen-Ketchum, Timothy S. Kern, Jena J. Steinle |
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| Rok vydání: | 2009 |
| Předmět: |
Retinal Ganglion Cells
medicine.medical_specialty medicine.medical_treatment Dopamine beta-Hydroxylase Biology Basement Membrane Retina Diabetes Mellitus Experimental Mice Cellular and Molecular Neuroscience Norepinephrine chemistry.chemical_compound Internal medicine medicine Dopamine beta hydroxylase deficiency Animals Mice Knockout Diabetic Retinopathy Retinal Vessels Retinal Diabetic retinopathy medicine.disease Sensory Systems Ophthalmology medicine.anatomical_structure Endocrinology Retinal ganglion cell Sympathectomy chemistry Pericyte Pericytes medicine.drug |
| Zdroj: | Experimental Eye Research. 88:1014-1019 |
| ISSN: | 0014-4835 |
| DOI: | 10.1016/j.exer.2008.12.015 |
| Popis: | Diabetes can cause damage to sympathetic nerves, and we have previously shown that experimental sympathectomy can produce capillary abnormalities in the retina similar to those seen in early diabetes. We postulate that the diabetes-induced loss of the sympathetic system, and at least in part the sympathetic neurotransmitter norepinephrine (NE), contributes to the development of retinal vascular and neural abnormalities in diabetes. Thus, we predict that non-diabetic animals that lack NE will develop microvascular and neural changes that are similar to those that are characteristic of diabetic retinopathy. To test this, retinas from non-diabetic dopamine beta hydroxylase (Dbh, Dbh(-/-)) knockout mice and their littermate controls were assessed for diabetic-like capillary and neural changes at 5 months of age. Genetic deletion of Dbh resulted in a significant decrease in retinal thickness and number of cells in the retinal ganglion cell layer (central retinal region). In addition, the number of pericyte ghosts and the basement membrane of retinal capillaries were significantly increased in the Dbh(-/-) mice. These results provide evidence that loss of sympathetic neurotransmission may contribute to the microvascular and neural changes of diabetic retinopathy. Restoration of sympathetic neurotransmission may be a new target for therapeutic intervention to inhibit the early phases of diabetic retinopathy. |
| Databáze: | OpenAIRE |
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