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Titolo:
Corticotropin-releasing hormone mediated neuroprotection against oxidativestress is associated with the increased release of non amyloidogenic amyloid beta precursor protein and with the suppression of nuclear factor-kappa B
Autore:
Lezoualch, F; Engert, S; Berning, B; Behl, C;
Indirizzi:
Max Planck Inst Psychiat, Independent Res Grp Neurodegenerat, D-80804 Munich, Germany Max Planck Inst Psychiat Munich Germany D-80804 D-80804 Munich, Germany
Titolo Testata:
MOLECULAR ENDOCRINOLOGY
fascicolo: 1, volume: 14, anno: 2000,
pagine: 147 - 159
SICI:
0888-8809(200001)14:1<147:CHMNAO>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED CELL-DEATH; ALZHEIMERS-DISEASE; TRANSCRIPTION FACTOR; BINDING-PROTEIN; HYDROGEN-PEROXIDE; HIPPOCAMPAL CELLS; INDUCED APOPTOSIS; FACTOR RECEPTORS; SECRETED FORMS; CRF RECEPTORS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
61
Recensione:
Indirizzi per estratti:
Indirizzo: Behl, C Max Planck Inst Psychiat, Independent Res Grp Neurodegenerat, D-80804 Munich, Germany Max Planck Inst Psychiat Munich Germany D-80804 Munich, Germany
Citazione:
F. Lezoualc'h et al., "Corticotropin-releasing hormone mediated neuroprotection against oxidativestress is associated with the increased release of non amyloidogenic amyloid beta precursor protein and with the suppression of nuclear factor-kappa B", MOL ENDOCR, 14(1), 2000, pp. 147-159

Abstract

The neuropeptide CRH is the central regulator of the hypothalamic-pituitary-adrenal (HPA) stress response system and is implicated in various stress-related conditions. In the neurodegenerative disorder Alzheimer's disease (AD), levels of CRH are decreased. AD pathology is characterized by the deposition of the nonsoluble amyloid beta protein (A beta), oxidative stress, and neuronal cell death. Employing primary neurons and clonal cells, we demonstrate that CRH has a neuroprotective activity in CRH-receptor type 1 (CRH-R1)-expressing neurons against oxidative cell death. The protective effectof CRH was blocked by selective and nonselective CRH-R1 antagonists and byprotein kinase A inhibitors. Overexpression of CRH-R1 in clonal hippocampal cells lacking endogenous CRH-receptors established neuroprotection by CRH. The activation of CRH-R1 and neuroprotection are accompanied by an increased release of non-amyloidogenic soluble A beta precursor protein. At the molecular level CRH caused the suppression of the DNA-binding activity and transcriptional activity of the transcription factor NF-kappa B. Suppressionof NF-kappa B by overexpression of a super-repressor mutant form of I kappa B-alpha, a specific inhibitor of NF-kappa B, led to protection of the cells against oxidative stress. These data demonstrate a novel cytoprotective effect of CRH that is mediated by CRH-R1 and downstream by suppression of NF-kappa B and indicate CRH as an endogenous protective neuropeptide againstoxidative cell death in addition to its function in the HPA-system. Moreover, the protective function of CRH proposes a molecular link between oxidative stress-related degenerative events and the CRH-R1 system.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/11/20 alle ore 00:57:58