Document Detail


Molecular cloning of a cell cycle regulation gene cyclin H from ischemic rat brain: expression in neurons after global cerebral ischemia.
MedLine Citation:
PMID:  10501206     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Gene expression plays an important role in determining the fate of neurons after ischemia. To identify additional genes that promote survival or execute programmed cell death in ischemic neurons, a subtractive cDNA library was constructed from hippocampus of rats subjected to global ischemia. With use of a differential screening technique, a cDNA was identified that was up-regulated after ischemia. The cDNA was found to have high homology with human cyclin H at both the nucleotide level (89%) and the amino acid level (93%). Northern blotting detected cyclin H mRNA in nonischemic and ischemic brains. In situ hybridization studies revealed that cyclin H message was found in hippocampal neurons in nonischemic brain. After ischemia, expression was increased primarily in the dentate gyrus and CA3 regions of hippocampus. Expression of cyclin H protein, detected by western blotting of hippocampal tissue, was increased after global ischemia, but expression of cyclins B1 and D1 and other related cell cycle genes (Cdk7 and Cdc2) was not increased. Cyclin H immunoreactivity was found exclusively within neurons. After ischemia, there was increased immunoreactivity within neurons in dentate gyrus, CA3, and cortex. Thus, cyclin H is expressed in normal postmitotic neurons and expression is increased in neurons that are ischemic yet survive. These results suggest that cyclin H may have functions in neurons other than cell cycle regulation, including other known functions such as DNA repair.
Authors:
K Jin; T Nagayama; J Chen; A R Stetler; K Kawaguchi; R P Simon; S H Graham
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of neurochemistry     Volume:  73     ISSN:  0022-3042     ISO Abbreviation:  J. Neurochem.     Publication Date:  1999 Oct 
Date Detail:
Created Date:  1999-10-14     Completed Date:  1999-10-14     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  2985190R     Medline TA:  J Neurochem     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1598-608     Citation Subset:  IM    
Affiliation:
Department of Neurology, University of Pittsburgh School of Medicine, Pennsylvania 15261, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Base Sequence
Brain / cytology,  metabolism*,  pathology
Cell Cycle / genetics*
Cloning, Molecular
Cyclin H
Cyclins / biosynthesis,  chemistry,  genetics*
Humans
Ischemic Attack, Transient / metabolism*,  pathology
Male
Molecular Sequence Data
Neurons / cytology,  metabolism*,  pathology
RNA, Messenger / genetics
Rats
Rats, Sprague-Dawley
Recombinant Proteins / biosynthesis,  chemistry
Sequence Alignment
Sequence Homology, Amino Acid
Transcription, Genetic*
Grant Support
ID/Acronym/Agency:
NS 24728/NS/NINDS NIH HHS; P01 NS35965/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/CCNH protein, human; 0/Ccnh protein, rat; 0/Cyclin H; 0/Cyclins; 0/RNA, Messenger; 0/Recombinant Proteins

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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