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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Gundimeda, Usha Mcneill, Thomas H. Schiffman, Jason Eric Gopalakrishna, Rayudu |
| Description | Author Affiliation: Gopalakrishna R ( Department of Cell and Neurobiology, University of Southern California, Los Angeles, CA 90089, USA. rgopalak@usc.edu) |
| Abstract | In this study, we have used the PC12 cell model to elucidate the mechanisms by which sublethal doses of oxidants induce neuritogenesis. The xanthine/xanthine oxidase (X/XO) system was used for the steady state generation of superoxide, and CoCl(2) was used as a representative transition metal redox catalyst. Upon treatment of purified protein kinase C (PKC) with these oxidants, there was an increase in its cofactor-independent activation. Redox-active cobalt competed with the redoxinert zinc present in the zinc-thiolates of the PKC regulatory domain and induced the oxidation of these cysteine-rich regions. Both CoCl(2) and X/XO induced neurite outgrowth in PC12 cells, as determined by an overexpression of neuronal marker genes. Furthermore, these oxidants induced a translocation of PKC from cytosol to membrane and subsequent conversion of PKC to a cofactor-independent form. Isoenzyme-specific PKC inhibitors demonstrated that PKCepsilon plays a crucial role in neuritogenesis. Moreover, oxidant-induced neurite outgrowth was increased with a conditional overexpression of PKCepsilon and decreased with its knock-out by small interfering RNA. Parallel with PKC activation, an increase in phosphorylation of the growth-associated neuronal protein GAP-43 at Ser(41) was observed. Additionally, there was a sustained activation of extracellular signal-regulated kinases 1 and 2, which was correlated with activating phosphorylation (Ser(133)) of cAMP-responsive element-binding protein. All of these signaling events that are causally linked to neuritogenesis were blocked by antioxidant N-acetylcysteine (both L and D-forms) and by a variety of PKC-specific inhibitors. Taken together, these results strongly suggest that sublethal doses of oxidants induce neuritogenesis via a direct redox activation of PKCepsilon. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 21 |
| Volume Number | 283 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2008-05-23 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cell Differentiation Drug Effects Neurons Cytology Enzymology Oxidants Pharmacology Protein Kinase C Metabolism Animals Antioxidants Chelating Agents Cobalt Cyclic AMP Response Element-Binding Protein Enzyme Activation Glutathione Isoenzymes MAP Kinase Signaling System Mitogen-Activated Protein Kinase 1 Mitogen-Activated Protein Kinase 3 Neurites Oxidation-Reduction PC12 Cells Phosphorylation Antagonists & Inhibitors Protein Kinase Inhibitors Sulfhydryl Compounds Zinc Research Support, N.I.H., Extramural Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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