Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Group I metabotropic glutamate receptors prevent endothelial programmed cell death independent from MAP kinase p38 activation in rat
Autore:
Lin, SH; Maiese, K;
Indirizzi:
Wayne State Univ, Sch Med, Lab Cellular & Mol Cerebral Ischemia, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 ral Ischemia, Detroit, MI 48201 USA Wayne State Univ, Sch Med, Dept Neurol, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 Dept Neurol, Detroit, MI 48201 USA Wayne State Univ, Sch Med, Dept Anat & Cell Biol, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 & Cell Biol, Detroit, MI 48201 USA Wayne State Univ, Sch Med, Ctr Mol Med & Genet, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 Med & Genet, Detroit, MI 48201 USA Wayne State Univ, Sch Med, Ctr Mol & Cellular Toxicol, Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 ular Toxicol, Detroit, MI 48201 USA
Titolo Testata:
NEUROSCIENCE LETTERS
fascicolo: 3, volume: 298, anno: 2001,
pagine: 207 - 211
SICI:
0304-3940(20010209)298:3<207:GIMGRP>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEURONAL APOPTOSIS; EXPRESSION; MODULATION;
Keywords:
apoptosis; DNA degradation; metabotropic glutamate receptors; nitric oxide; phosphatidylserine residues; primary endothelial cell culture;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
15
Recensione:
Indirizzi per estratti:
Indirizzo: Maiese, K Wayne State Univ, Sch Med, Lab Cellular & Mol Cerebral Ischemia,Detroit, MI 48201 USA Wayne State Univ Detroit MI USA 48201 ia, Detroit, MI 48201 USA
Citazione:
S.H. Lin e K. Maiese, "Group I metabotropic glutamate receptors prevent endothelial programmed cell death independent from MAP kinase p38 activation in rat", NEUROSCI L, 298(3), 2001, pp. 207-211

Abstract

Activation of Group I metabotropic glutamate receptors (mGluRs) prevents neuronal programmed cell death (PCD), but the role of these receptors in thevascular endothelial cell (EC) system has not been defined. Since ECs are principal targets for ischemic free radical injury, we examined whether themGluR system could modulate vascular PCD. Activation of the Group I mGluR system, but not antagonism, addressed two distinct pathways of PCD by preventing the destruction of genomic DNA and maintaining EC membrane asymmetry. The induction of nitric oxide (NO)-induced PCD in ECs paralleled the specific activation of the MAP kinase p38 pathway, but the vascular protection conferred by the Group I mGluR system appears to rely on more downstream cellular pathways. We provide initial evidence for Group I mGluRs to prevent NO-induced vascular injury and offer new directions for vascular disease treatment. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 11/07/20 alle ore 20:44:52