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Increased neuronal glutathione and neuroprotection in GTRAP3-18-deficient mice.

Abstract：

:Glutathione (GSH) is an important neuroprotective molecule in the brain. The strategy to increase neuronal GSH level is a promising approach to the treatment of neurodegenerative diseases. However, the regulatory mechanism by which neuron-specific GSH synthesis is facilitated remains elusive. Glutamate transporter-associated protein 3-18 (GTRAP3-18) is an endoplasmic reticulum protein interacting with excitatory amino acid carrier 1 (EAAC1), which is a neuronal glutamate/cysteine transporter. To investigate the potential regulatory mechanism to increase neuronal GSH level in vivo, we generated GTRAP3-18-deficient (GTRAP3-18(-/-)) mice using a gene-targeting approach. Disruption of the GTRAP3-18 gene resulted in increased EAAC1 expression in the plasma membrane, increased neuronal GSH content and neuroprotection against oxidative stress. In addition, GTRAP3-18(-/-) mice performed better in motor/spatial learning and memory tests than wild-type mice. Therefore, the suppression of GTRAP3-18 increases neuronal resistance to oxidative stress by increasing GSH content and also facilitates cognitive function. The present results may provide a molecular basis for the development of treatments for neurodegenerative diseases.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Aoyama K,Wang F,Matsumura N,Kiyonari H,Shioi G,Tanaka K,Kinoshita C,Kikuchi-Utsumi K,Watabe M,Nakaki T

doi

10.1016/j.nbd.2011.12.016

subject

Has Abstract

pub_date

2012-03-01 00:00:00

pages

973-82

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(11)00391-3

journal_volume

45

pub_type

杂志文章

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