Activation of Protein Kinase C by Trimethyltin: Relevance to Neurotoxicity
Benzophenanthridines
0301 basic medicine
Microscopy, Confocal
Cell Death
Trimethyltin Compounds
Blotting, Western
Neurotoxins
Cell Differentiation
Immunohistochemistry
PC12 Cells
Phenanthridines
Rats
Enzyme Activation
03 medical and health sciences
Alkaloids
Animals
Tissue Distribution
Protein Kinase C
DOI:
10.1046/j.1471-4159.1995.65052338.x
Publication Date:
2010-07-15T23:54:40Z
AUTHORS (5)
ABSTRACT
Abstract: The differentiated PC12 cell neuronal model was used to determine the effect of trimethyltin (TMT) on protein kinase C (PKC). Cells treated with 5–20 µM TMT showed a partial and sustained PKC translocation within 30 min and persisted over a 24‐h period. TMT treatment was accompanied by a low level of PKC down‐regulation over 24 h, which was small compared with that produced by phorbol esters. Confocal imaging of differentiated PC12 cells showed that PKC translocates to the plasma membrane and the translocation is blocked by the PKC inhibitor chelerythrine (1 µM). Phorbol myristate‐induced PKC down‐regulation or inhibition with chelerythrine provided protection against TMT‐induced cytotoxicity. It was concluded that TMT‐induced PKC translocation and activation contribute to the cytotoxicity of TMT in differentiated PC12 cells.
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