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19. Nuclear factor-kappaB-dependent cyclin D1 induction and DNA replication associated with N-methyl-D-aspartate receptor-mediated apoptosis in rat striatum.

Author

Liang ZQ, Wang X, Li LY, Wang Y, Chen RW, Chuang DM, Chase TN, and Qin ZH

Subjects
Analysis of Variance, Animals, Apoptosis drug effects, Bromodeoxyuridine metabolism, Cyclin-Dependent Kinase 4 metabolism, DNA Replication drug effects, Dose-Response Relationship, Drug, Drug Interactions, Enzyme Activation drug effects, Enzyme Inhibitors pharmacology, Functional Laterality, In Situ Nick-End Labeling methods, Neurons drug effects, Peptides pharmacology, Phosphopyruvate Hydratase metabolism, Quinolinic Acid pharmacology, Rats, Rats, Sprague-Dawley, Apoptosis physiology, Corpus Striatum cytology, Cyclin D1 metabolism, DNA Replication physiology, NF-kappa B metabolism, Neurons physiology, Receptors, N-Methyl-D-Aspartate physiology
Abstract

Cell cycle reentry has been found during apoptosis of postmitotic neurons under certain pathological conditions. To evaluate whether nuclear factor-kappaB (NF-kappaB) activation promotes cell cycle entry and neuronal apoptosis, we studied the relation among NF-kappaB-mediated cyclin induction, bromodeoxyuridine (BrdU) incorporation, and apoptosis initiation in rat striatal neurons following excitotoxic insult. Intrastriatally injected N-methyl-D-aspartate receptor agonist quinolinic acid (QA, 60 nmol) elicited a rise in cyclin D1 mRNA and protein levels (P<0.05). QA-induced NF-kappaB activation occurred in striatal neurons and nonneuronal cells and partially colocalized with elevated cyclin D1 immunoreactivity and TUNEL-positive nuclei. QA triggered DNA replication as evidenced by BrdU incorporation; some striatal BrdU-positive cells were identified as neurons by colocalization with NeuN. Blockade of NF-kappaB nuclear translocation with the recombinant peptide NF-kappaB SN50 attenuated the QA-induced elevation in cyclin D1 and BrdU incorporation. QA-induced internucleosomal DNA fragmentation was blunted by G(1)/S-phase cell cycle inhibitors. These findings suggest that NF-kappaB activation stimulates cyclin D1 expression and triggers DNA replication in striatal neurons. Excitotoxin-induced neuronal apoptosis may thus result from, at least partially, a failed cell cycle attempt., ((c) 2007 Wiley-Liss, Inc.)

Published
2007
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