PKC delta mediates paraquat-induced Nox1 expression in dopaminergic neurons

    Authors

    A. C. Cristovao; J. Barata; G. Je;Y. S. Kim

    Comments

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    Abbreviated Journal Title

    Biochem. Biophys. Res. Commun.

    Keywords

    NADPH oxidase; Paraquat; Protein Kinase C delta; Parkinson Disease; KINASE-C-DELTA; SMOOTH-MUSCLE-CELLS; NADPH OXIDASE; PARKINSONS-DISEASE; OXIDATIVE STRESS; POSSIBLE INVOLVEMENT; MICROGLIAL CELLS; SUBSTANTIA-NIGRA; REACTIVE OXYGEN; HUMAN MONOCYTES; Biochemistry & Molecular Biology; Biophysics

    Abstract

    Our previous works have shown that the (NADPH) oxidase (Nox) enzyme, in particular Nox1, plays an important role in oxidative stress and subsequent dopaminergic cell death elicited by paraquat (PQ). In non-neuronal and glial cells, protein kinase C delta (PKC delta) shows the ability to regulate the activity of the Nox system. Herein we aimed to investigate if also in dopaminergic neurons exposed to PQ, PKC delta can regulate Nox1 expression. The chemical inhibitor, rottlerin, and short interference RNA (siRNA) were used to inhibit or selectively knockdown PKC delta, respectively. The studies were performed using the immortalized rat mesencephalic dopaminergic cell line (N27 cells) exposed to PQ after pre-incubation with rottlerin or transfected with PKC delta-siRNA. We observed that inhibition or knockdown of PKC delta significantly reduced PQ induced Nox1 transcript and protein levels, ROS generation and subsequent dopaminergic cell death. The results suggest that PKC delta plays a role in the regulation of Nox1-mediated oxidative stress elicited by PQ and could have a role in the pathogenesis of Parkinson's disease. (C) 2013 Elsevier Inc. All rights reserved.

    Journal Title

    Biochemical and Biophysical Research Communications

    Volume

    437

    Issue/Number

    3

    Publication Date

    1-1-2013

    Document Type

    Article

    Language

    English

    First Page

    380

    Last Page

    385

    WOS Identifier

    WOS:000323016500009

    ISSN

    0006-291X

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