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Protein kinase C-β mediates neuronal activation of Na(+)/H(+) exchanger-1 during glutamate excitotoxicity.

Abstract：

:Na(+)/H(+) exchanger-1 (NHE-1) activity is known to play a critical role in the neuronal injury caused by glutamate. However, the underlying mechanism is not clear. This study shows that NHE-1 activation and its phosphorylation during glutamate exposure were attenuated by the inhibition of protein kinase C (PKC)-βI and -βII, leading to reduced neuronal death. In addition, activations of PKC-βI and -βII by PKC-βI and -βII CAT plasmid or by PMA, PKC-β pharmacological activator have stimulated the activity and phosphorylation of NHE-1, which were abolished by inhibition of PKC-β in neuronal cells. Furthermore, the inhibition of PKC-β has mediated neuroprotective effect on glutamate-induced cells, which is similar to neuroprotective efficacy of siRNA NHE-1 transfection. Taken together, these results suggest that activation of the PKC-βI and -βII pathway by glutamate increases the activity and phosphorylation of NHE-1, and that these increases contribute to neuronal cell death. In this study, we demonstrate that PKC-βI and -βII are involved in the regulation of NHE-1 activation following glutamate exposure in neuron.

journal_name

Cell Signal

journal_title

Cellular signalling

authors

Lee BK,Yoon JS,Lee MG,Jung YS

doi

10.1016/j.cellsig.2013.12.011

subject

Has Abstract

pub_date

2014-04-01 00:00:00

pages

697-704

issue

4

eissn

0898-6568

issn

1873-3913

pii

S0898-6568(13)00392-6

journal_volume

26

pub_type

杂志文章

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