Fragmentation of Protein Kinase N (PKN) in the Hydrocephalic Rat Brain

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Author(s)

    • OKII Norifumi
    • Department of Neurosurgery, Graduate School of Biomedical Sciences, Hiroshima University
    • AMANO Taku
    • Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical Sciences, Hiroshima University
    • SEKI Takahiro
    • Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical Sciences, Hiroshima University
    • MATSUBAYASHI Hiroaki
    • Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical Sciences, Hiroshima University
    • KURISU Kaoru
    • Department of Neurosurgery, Graduate School of Biomedical Sciences, Hiroshima University
    • SAKAI Norio
    • Department of Molecular and Pharmacological Neuroscience, Graduate School of Biomedical Sciences, Hiroshima University

Abstract

PKN (protein kinase N; also called protein kinase C-related kinase (PRK-1)), is a serine/threonine protein kinase that is ubiquitously expressed in several organs, including the brain. PKN has a molecular mass of 120 kDa and has two domains, a regulatory and a catalytic domain, in its amino-terminals and carboxyl-terminus, respectively. Although the role of PKN has not been fully elucidated, previous studies have revealed that PKN is cleaved to a constitutively active catalytic fragment of 55 kDa in response to apoptotic signals. Hydrocephalus is a pathological condition caused by insufficient cerebrospinal fluid (CSF) circulation and subsequent excess of CSF in the brain. In this study, in order to elucidate the role of PKN in the pathophysiology of hydrocephalus, we examined PKN fragmentation in hydrocephalic model rats.<br> Hydrocephalus was induced in rats by injecting kaolin into the cisterna magna. Kaolin-induced rats (n=60) were divided into three groups according to the observation period after treatment (group 1: 3–6 weeks, group 2: 7–12 weeks, and group 3: 13–18 weeks). Sham-treated control rats, injected with sterile saline (n=20), were similarly divided into three groups. Spatial learning ability was estimated by a modified water maze test. Thereafter, brains were cut into slices and ventricular dilatation was estimated. Fragmentation of PKN was observed by Western blotting in samples collected from the parietal cortex, striatum, septal nucleus, hippocampus, and periaqueductal gray matter.<br> All kaolin-induced rats showed ventricular dilatation. Most of them showed less spatial learning ability than those of sham-treated controls. In most regions, fragmentation of PKN had occurred in a biphasic manner more frequently than that in controls. The appearance of PKN fragmentation in periaqueductal gray matter was correlated with the extent of ventricular dilation and spatial learning disability. These results revealed that PKN fragmentation was observed in rats with kaolin-induced hydrocephalus, models for chronically-damaged brain dysfunction, suggesting that persistent brain insult, such as apoptosis, had occurred in these models. PKN fragmentation could be a hallmark for evaluating morphological and functional damage of the hydrocephalus.<br>

Journal

  • ACTA HISTOCHEMICA ET CYTOCHEMICA

    ACTA HISTOCHEMICA ET CYTOCHEMICA 40(1), 113-121, 2007-02-28

    JAPAN SOCIETY OF HISTOCHEMISTRY AND CYTOCHEMISTRY

References:  29

Codes

  • NII Article ID (NAID)
    110006633421
  • NII NACSIS-CAT ID (NCID)
    AA00508022
  • Text Lang
    ENG
  • Article Type
    ART
  • ISSN
    00445991
  • Data Source
    CJP  NII-ELS  J-STAGE  NDL-Digital 
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