Increased cyclin D1 in vulnerable neurons in the hippocampus after ischaemia and epilepsy: a modulator of in vivo programmed cell death?

Autor: Timsit, Serge, Rivera, Santiago, Ouaghi, Philippe, Guischard, Frédérique, Tremblay, Evelyne, Ben-Ari, Yehezkel, Khrestchatisky, Michel
Přispěvatelé: Epilepsie et Ischemie Cerebrale, Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Tyzio, Roman
Jazyk: angličtina
Rok vydání: 1999
Předmět:
Male
MESH: Cyclin D1
MESH : RNA
Messenger
Time Factors
MESH: Hippocampus
MESH: Cyclin D2
MESH: Cyclin D3
MESH: Neurons
Gene Expression
Apoptosis
MESH: Cell Cycle
MESH : Hippocampus
Hippocampus
MESH: Nerve Degeneration
Brain Ischemia
MESH: Prosencephalon
MESH: Amygdala
Excitatory Amino Acid Agonists
Cyclin D2
Cyclin D1
MESH: Animals
Cyclin D3
In Situ Hybridization
Neurons
MESH : Cell Nucleus
Kainic Acid
MESH : Rats
MESH : Epilepsy
Cell Cycle
MESH : In Situ Hybridization
MESH: Brain Ischemia
Amygdala
MESH : Cyclin D1
MESH : Cyclin D2
MESH : Cyclin D3
MESH : Nerve Degeneration
MESH: Epilepsy
MESH : Time Factors
MESH: Cell Nucleus
MESH: Gene Expression
MESH: Rats
MESH : Male
MESH : Cyclins
Neurotoxins
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
MESH : Rats
Wistar
MESH : Neurotoxins
MESH : Neurons
Prosencephalon
MESH: In Situ Hybridization
Cyclins
MESH : Cell Cycle
Animals
RNA
Messenger
Rats
Wistar
[SDV.BC] Life Sciences [q-bio]/Cellular Biology
MESH : Prosencephalon
MESH: Neurotoxins
MESH: RNA
Messenger
MESH : Excitatory Amino Acid Agonists
Cell Nucleus
Epilepsy
MESH : Amygdala
[ SDV.BC ] Life Sciences [q-bio]/Cellular Biology
MESH: Apoptosis
MESH: Time Factors
MESH: Biological Markers
MESH: Rats
Wistar
MESH: Kainic Acid
MESH: Cyclins
MESH: Male
Rats
MESH : Gene Expression
MESH : Biological Markers
MESH : Kainic Acid
nervous system
MESH : Brain Ischemia
Nerve Degeneration
MESH : Animals
MESH: Excitatory Amino Acid Agonists
MESH : Apoptosis
Biomarkers
Zdroj: European Journal of Neuroscience
European Journal of Neuroscience, Wiley, 1999, 11 (1), pp.263-78
ISSN: 0953-816X
1460-9568
Popis: International audience; Several observations suggest that delayed neuronal death in ischaemia, epilepsy and other brain disorders includes an apoptotic component, involving programmed cell death (PCD). PCD is hypothesized to result, in part, from aberrant control of the cell cycle. Because they are instrumental in mitosis, cyclins D are key markers to evaluate whether neurons indeed progress into the cell cycle in situations of pathology. Therefore, we investigated in rat brains, the expression of cyclins D in the delayed neuronal death that occurs following transient global ischaemia and kainate-induced seizures. Following a four-vessel occlusion insult, quantitative in situ hybridization revealed a highly significant and persistent 100% increase of cyclin D1 mRNA in the vulnerable pyramidal neurons of the CA1 hippocampal region. Ischaemia also induced a smaller and transient cyclin D1 mRNA increase in the resistant CA3 area and dentate gyrus. In contrast, the cyclin D2 and D3 mRNAs, expressed constitutively in the adult rat hippocampus, were not upregulated. Following kainate-induced seizures, cyclin D1 mRNA was induced in the vulnerable CA3 region, and to a lesser extent, in non-vulnerable regions. Cyclin D1 immunohistochemistry revealed increased protein levels in the cytoplasm and nucleus of neurons commited to die after ischaemia. Double labelling experiments indicate that cyclin D1 is also expressed in reactive astrocytes but not in microglial cells. Finally, we report that in neurons, cyclin D1 expression peaks before nuclear condensation and the appearance of DNA fragmentation. We propose that cyclin D1, when expressed at high levels in lesioned neurons, may act as a modulator of apoptosis.
Databáze: OpenAIRE
Externí odkaz: