Medizinische Universität Graz Austria/Österreich - Forschungsportal - Medical University of Graz
Gewählte Publikation:
Graier, WF; Grubenthal, I; Dittrich, P; Wascher, TC; Kostner, GM.
Intracellular mechanism of high D-glucose-induced modulation of vascular cell proliferation.
Eur J Pharmacol. 1995; 294(1):221-229
Doi: 10.1016%2F0014-2999%2895%2900534-X
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- Führende Autor*innen der Med Uni Graz
- Graier Wolfgang
- Co-Autor*innen der Med Uni Graz
- Kostner Gerhard
- Wascher Thomas
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- Abstract:
- Development of atherosclerosis in diabetes patients is thought to be associated with high D-glucose-induced changes in vascular cell proliferation. This study was designed to investigate the intracellular mechanisms of altered proliferation in porcine aortic endothelial and smooth muscle cells under high D-glucose conditions. Two different technical approaches were used for determination of cell proliferation, a cell counting procedure and bromodeoxyuridine incorporation. D-Glucose diminished endothelial cell proliferation (30.3%) and increased smooth muscle cell proliferation (143%) in a dose-dependent manner. Neither D-mannitol, sucrose nor L-glucose mimicked the effect of D-glucose. Inhibition of D-glucose uptake into vascular cells by cytochalasin B prevented the effect of high D-glucose on cell proliferation. The aldose-reductase inhibitors, sorbinil and zopolrestat, little affected high D-glucose-attenuated endothelial cell proliferation, while the enhanced proliferation of smooth muscle cells was prevented by aldose-reductase inhibitors. Elevation of cellular glutathione levels yielded protection of both cell types from high D-glucose-mediated changes in cell proliferation, suggesting that high D-glucose may act via generation of oxidative species. Finally, aminoguanidine was shown to constitute a very potent inhibitor of D-glucose-induced dysfunction in vascular cell proliferation. These data suggest that high D-glucose-induced changes in cell proliferation of endothelial and smooth muscle cells are related to specific D-glucose uptake rather than hyperosmolality. Aldose-reductase seems to be mainly involved in the effect of high D-glucose only on smooth muscle cell proliferation, while in endothelial cells there is (are) other factor(s) in addition to the sorbitol pathway involved in high D-glucose-induced changes in cell proliferation.
- Find related publications in this database (using NLM MeSH Indexing)
- Aldehyde Reductase - antagonists and inhibitors
- Animals - antagonists and inhibitors
- Cell Division - drug effects
- Cells, Cultured - drug effects
- Cytochalasin B - pharmacology
- Diuretics, Osmotic - pharmacology
- Endothelium, Vascular - cytology
- Enzyme Inhibitors - pharmacology
- Glucose - metabolism
- Glutathione - pharmacology
- Guanidines - pharmacology
- Mannitol - pharmacology
- Muscle, Smooth, Vascular - cytology
- Osmolar Concentration - cytology
- Oxidation-Reduction - cytology
- Sucrose - pharmacology
- Swine - pharmacology
- Xanthine Oxidase - antagonists and inhibitors
- Find related publications in this database (Keywords)
- Endothelial Cell
- Smooth Muscle Cell
- Diabetes Mellitus
- Atherosclerosis
- Aminoguanidine
- Glutathione
- Aldose-Reductase