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Activation of protein kinase C-delta attenuates kainate-induced cell death of cortical neurons.

Authors
Jung, YS; Lee, BK; Park, HS; Shim, JK; Kim, SU; Lee, SH; Baik, EJ; Moon, CH
Citation
Neuroreport, 16(7):741-744, 2005
Journal Title
Neuroreport
ISSN
0959-49651473-558X
Abstract
We investigated the role of individual protein kinase C (PKC) isoforms during kainate toxicity in cortical neurons. Treatment with 50 microM kainate induced isoform-specific activation of PKC-delta according to the translocation from the soluble to the particulate fraction, while it caused remarkable decreases in PKC alpha, beta, epsilon and zeta in both fractions. Kainate-induced neuronal death was significantly increased by pharmacological inhibition of PKC-delta with rottlerin, suggesting a protective role of PKC-delta against kainate toxicity. A PKC activator phorbol 12-myristate 13-acetate remarkably attenuated the kainate-induced neuronal death. Although phorbol 12-myristate 13-acetate activates PKC-epsilon and PKC-delta, the protective effect of phorbol 12-myristate 13-acetate was almost completely abolished by rottlerin, but not by epsilonV1-2. These results suggest that activation of PKC-delta attenuates the kainate-induced cell death of cortical neurons.
MeSH terms
AnimalsCarcinogens/pharmacologyCell Death/drug effectsCell Death/physiology*Cells, CulturedCerebral Cortex/cytologyExcitatory Amino Acid Agonists/toxicityIntracellular Signaling Peptides and Proteins/pharmacologyKainic Acid/toxicityMiceNeurons/cytology*Neurons/enzymology*Protein Kinase C/antagonists & inhibitorsProtein Kinase C/metabolism*Protein Kinase C-deltaTetradecanoylphorbol Acetate/pharmacology
PMID
15858417
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Physiology
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
정, 이숙김, 승업이, 수환백, 은주문, 창현
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