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Titolo:
Cyclin-dependent kinase 4 and cyclin D1 are required for excitotoxin-induced neuronal cell death in vivo
Autore:
Ino, H; Chiba, T;
Indirizzi:
Chiba Univ, Grad Sch Med, Dept Neurobiol C1, Chuo Ku, Chiba 2608670, JapanChiba Univ Chiba Japan 2608670 urobiol C1, Chuo Ku, Chiba 2608670, Japan
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 16, volume: 21, anno: 2001,
pagine: 6086 - 6094
SICI:
0270-6474(20010815)21:16<6086:CK4ACD>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
INDUCED APOPTOSIS; GENE-EXPRESSION; DNA-DAMAGE; SELECTIVE INDUCTION; SYMPATHETIC NEURONS; ALZHEIMERS-DISEASE; ESTROGEN-RECEPTOR; PROMOTE SURVIVAL; FAMILY MEMBERS; NERVOUS-SYSTEM;
Keywords:
CDK4; cyclin D1; cyclin-dependent kinases; cyclins; neuronal cell death; kainate; phosphorothioate antisense; oligonucleotides;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Ino, H Chiba Univ, Grad Sch Med, Dept Neurobiol C1, Chuo Ku, 1-8-1 Inohana, Chiba2608670, Japan Chiba Univ 1-8-1 Inohana Chiba Japan 2608670 , Chiba2608670, Japan
Citazione:
H. Ino e T. Chiba, "Cyclin-dependent kinase 4 and cyclin D1 are required for excitotoxin-induced neuronal cell death in vivo", J NEUROSC, 21(16), 2001, pp. 6086-6094

Abstract

Systemic administration of the glutamic acid analog kainic acid (KA) causes neuronal cell death in brain-vulnerable regions, such as the piriform cortex, hippocampus, and amygdala in rats. We investigated the relationship between the KA-induced neuronal apoptosis and expression of cyclin-dependent kinase 4 (CDK4) and cyclin D1, key regulators of cell cycle progression. Expression of CDK4 and cyclin D1 was upregulated in neurons of the rat piriform cortex and amygdala 1-3 d after KA administration in vivo. CDK4 and cyclin D1 proteins were induced in the cytoplasm and nuclei of neurons, with a concomitant increase of CDK4- and cyclin D1-positive microglia in the affected areas. Continuous infusion of 100 muM CDK4 or cyclin D1 antisense oligonucleotides into the lateral ventricle using mini-osmotic pumps suppressed the excitotoxin-induced neuronal cell death in the piriform cortex and basolateral amygdaloid nucleus, whereas sense oligonucleotides exhibited no such effect. Although KA administration causes prolonged c-Fos expression in the vulnerable regions that preceded the induction of neuronal apoptosis, the CDK4 or cyclin D1 antisense oligonucleotides exhibited no suppressive effect on c-Fos levels. Our results suggest that CDK4 and cyclin D1 are essential for KA-induced neuronal apoptosis in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 09:02:35