Aberrant δPKC activation in the spinal cord of Wobbler mouse: A model of motor neuron disease

Kunjan R. Dave; Ami P. Raval; Jesús Purroy; Ilias G. Kirkinezos; Carlos T. Moraes; Walter G. Bradley; Miguel A. Pérez-Pinzón

doi:10.1016/j.nbd.2004.08.017

Aberrant δPKC activation in the spinal cord of Wobbler mouse: A model of motor neuron disease

Kunjan R. Dave, Ami P. Raval, Jesús Purroy, Ilias G. Kirkinezos, Carlos T. Moraes, Walter G. Bradley, Miguel A. Pérez-Pinzón

Neurology

Research output: Contribution to journal › Article

13 Scopus citations

Abstract

Protein kinase C (PKC) was suggested to play a role in the pathology of amyotrophic lateral sclerosis (ALS) patients. Activation of PKC delta (δPKC) modulates mitochondrially induced apoptosis. The goal of the present study was to define whether δPKC activation occurs in Wobbler mouse spinal cord (a model of motor neuron disease). The level of δPKC in the soluble fraction was significantly decreased in the spinal cord of Wobbler mice, which was associated with a significant increase in δPKC cleavage. Since caspase-3 is known to cleave δPKC, we determined caspase-3 activation in the Wobbler mice spinal cord, immunohistochemically. The results demonstrated intense immunoreactivity for activated caspase-3 in corticospinal tract motor neurons of Wobbler mice spinal cord. We hypothesize from these results that caspase-3 activation cleaves δPKC, which in turn promotes an aberrant signal transduction pathway in the Wobbler spinal cord.

Original language	English (US)
Pages (from-to)	126-133
Number of pages	8
Journal	Neurobiology of Disease
Volume	18
Issue number	1
DOIs	https://doi.org/10.1016/j.nbd.2004.08.017
State	Published - Feb 1 2005

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Keywords

Amyotrophic lateral sclerosis
Apoptosis
Cytochrome c
Immunohistochemistry
Neurological disorders
Neuronal death
SOD1 mice

ASJC Scopus subject areas

Neurology

Cite this

Dave, K. R., Raval, A. P., Purroy, J., Kirkinezos, I. G., Moraes, C. T., Bradley, W. G., & Pérez-Pinzón, M. A. (2005). Aberrant δPKC activation in the spinal cord of Wobbler mouse: A model of motor neuron disease. Neurobiology of Disease, 18(1), 126-133. https://doi.org/10.1016/j.nbd.2004.08.017

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abstract = "Protein kinase C (PKC) was suggested to play a role in the pathology of amyotrophic lateral sclerosis (ALS) patients. Activation of PKC delta (δPKC) modulates mitochondrially induced apoptosis. The goal of the present study was to define whether δPKC activation occurs in Wobbler mouse spinal cord (a model of motor neuron disease). The level of δPKC in the soluble fraction was significantly decreased in the spinal cord of Wobbler mice, which was associated with a significant increase in δPKC cleavage. Since caspase-3 is known to cleave δPKC, we determined caspase-3 activation in the Wobbler mice spinal cord, immunohistochemically. The results demonstrated intense immunoreactivity for activated caspase-3 in corticospinal tract motor neurons of Wobbler mice spinal cord. We hypothesize from these results that caspase-3 activation cleaves δPKC, which in turn promotes an aberrant signal transduction pathway in the Wobbler spinal cord.",

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AB - Protein kinase C (PKC) was suggested to play a role in the pathology of amyotrophic lateral sclerosis (ALS) patients. Activation of PKC delta (δPKC) modulates mitochondrially induced apoptosis. The goal of the present study was to define whether δPKC activation occurs in Wobbler mouse spinal cord (a model of motor neuron disease). The level of δPKC in the soluble fraction was significantly decreased in the spinal cord of Wobbler mice, which was associated with a significant increase in δPKC cleavage. Since caspase-3 is known to cleave δPKC, we determined caspase-3 activation in the Wobbler mice spinal cord, immunohistochemically. The results demonstrated intense immunoreactivity for activated caspase-3 in corticospinal tract motor neurons of Wobbler mice spinal cord. We hypothesize from these results that caspase-3 activation cleaves δPKC, which in turn promotes an aberrant signal transduction pathway in the Wobbler spinal cord.

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10.1016/j.nbd.2004.08.017