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Staurosporine Induces ROS-Mediated Process Formation in Human Gingival Fibroblasts and Rat Cortical Astrocytes

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In the present study, we investigated the effect ofstaurosporine on the formation of cellular processes in humangingival fibroblasts and rat astrocytes. Staurosporine caused arapid induction of process formation in human gingivalfibroblasts and rat astrocytes in a concentration dependentmanner. The process formation of human gingival fibroblastsand rat astrocytes was prevented by the pretreatment withN-acetylcysteine, suggesting that staurosporine-induced ROSproduction was responsible for the process formation. Colchicine, a microtubule depolymerizing agent, inhibited thestaurosporine-induced process formation, whereas cytochalasinD, an actin filament breakdown agent, failed to suppress theformation of cellular processes. This result indicated thatpolymerization of microtubule, and not actin filament, wasresponsible for the formation of cellular processes induced bystaurosporine. In support of this hypothesis, Western blotanalysis was conducted using anti-tubulin antibody, and theresults showed that the amount of polymerized microtubule wasincreased by the treatment with staurosporine while that ofdepolymerized beta-tubulin in soluble fraction was decreased. These results indicate that staurosporine induces ROSmediated,microtubule-dependent formation of cellularprocesses in human gingival fibroblasts and rat astrocytes.

Abstract

In the present study, we investigated the effect ofstaurosporine on the formation of cellular processes in humangingival fibroblasts and rat astrocytes. Staurosporine caused arapid induction of process formation in human gingivalfibroblasts and rat astrocytes in a concentration dependentmanner. The process formation of human gingival fibroblastsand rat astrocytes was prevented by the pretreatment withN-acetylcysteine, suggesting that staurosporine-induced ROSproduction was responsible for the process formation. Colchicine, a microtubule depolymerizing agent, inhibited thestaurosporine-induced process formation, whereas cytochalasinD, an actin filament breakdown agent, failed to suppress theformation of cellular processes. This result indicated thatpolymerization of microtubule, and not actin filament, wasresponsible for the formation of cellular processes induced bystaurosporine. In support of this hypothesis, Western blotanalysis was conducted using anti-tubulin antibody, and theresults showed that the amount of polymerized microtubule wasincreased by the treatment with staurosporine while that ofdepolymerized beta-tubulin in soluble fraction was decreased. These results indicate that staurosporine induces ROSmediated,microtubule-dependent formation of cellularprocesses in human gingival fibroblasts and rat astrocytes.

참고문헌 (24)

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