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Neuroprotection mediated by glutamate carboxypeptidase II (NAALADase) inhibition requires TGF-beta.

Abstract：

:Inhibition of glutamate carboxypeptidase (GCP) II (EC 3.4.17.21), also termed N-acetylated alpha-linked acidic dipeptidase (NAALADase), has been shown to protect against ischemic injury presumably via decreasing glutamate and increasing N-acetyl-aspartyl-glutamate (NAAG). NAAG is a potent and selective mGlu3 receptor agonist. Activation of glial mGlu3 receptors has been shown to protect against NMDA toxicity by releasing transforming growth factors, TGF-betas. We hypothesized that GCP II inhibition could be neuroprotective also via TGF-betas, due to increased NAAG. To verify this, Enzyme-Linked Immunosorbent Assays (ELISAs) were performed on media from both control and ischemic cultures treated with the GCP II inhibitor, 2-(phosphonomethyl)-pentanedioic acid (2-PMPA). We found that 2-PMPA attenuated ischemia-induced declines in TGF-beta. To further assess the role of TGF-betas in 2-PMPA-mediated neuroprotection, a neutralizing antibody to TGF-beta (TGF-beta Ab) was used. In both in vitro and in vivo models of cerebral ischemia, TGF-beta Ab reversed the neuroprotection by 2-PMPA. Antibodies to other growth factors had no effect. Data suggests that neuroprotection by GCP II inhibition may be partially mediated by promoting TGF-beta release.

journal_name

Eur J Pharmacol

journal_title

European journal of pharmacology

authors

Thomas AG,Liu W,Olkowski JL,Tang Z,Lin Q,Lu XC,Slusher BS

doi

10.1016/s0014-2999(01)01239-0

keywords:

subject

Has Abstract

pub_date

2001-10-26 00:00:00

pages

33-40

issue

1

eissn

0014-2999

issn

1879-0712

pii

S0014299901012390

journal_volume

430

pub_type

杂志文章

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