Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2003-12-17
pubmed:abstractText
Intermittent hypoxia (IH) during sleep induces temporally defined increases in apoptosis within vulnerable brain regions such as the hippocampal CA1 region in rats. Protein kinase B (AKT) has emerged as major signal transduction protein underlying inhibition of apoptosis and consequent increases in cell survival. Sprague Dawley adult male rats were exposed during sleep to IH or to normoxia (RA) for periods ranging from 0 to 30 days, and expression of total and phosphorylated AKT, of forkhead family members FKHR and FKHRL1, and of glycogen synthase kinase 3beta (GSK3beta) was assessed. Decreases in phosphorylation occurred as early as 1 h IH exposure, reached a nadir at 6 h-3 days, and then progressively returned to baseline levels at 14-30 days. Phosphorylated AKT and GSK3beta were intensely expressed and highly colocalized within neuronal cells (Neu-N positive) in the CA1 region. Thus, IH induces time-dependent biphasic changes in AKT survival pathways within the CA1 region that are temporally correlated with the initial increases and subsequent decreases in neuronal apoptosis.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Akt1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/Foxo1 protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Foxo1a protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Foxo3a protein, rat, http://linkedlifedata.com/resource/pubmed/chemical/Glycogen Synthase Kinase 3, http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Serine-Threonine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-akt, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/glycogen synthase kinase 3 beta
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0969-9961
pubmed:author
pubmed:issnType
Print
pubmed:volume
14
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
440-6
pubmed:dateRevised
2011-11-2
pubmed:meshHeading
pubmed-meshheading:14678760-Animals, pubmed-meshheading:14678760-Apoptosis, pubmed-meshheading:14678760-Cell Survival, pubmed-meshheading:14678760-DNA-Binding Proteins, pubmed-meshheading:14678760-Disease Models, Animal, pubmed-meshheading:14678760-Down-Regulation, pubmed-meshheading:14678760-Forkhead Transcription Factors, pubmed-meshheading:14678760-Glycogen Synthase Kinase 3, pubmed-meshheading:14678760-Hippocampus, pubmed-meshheading:14678760-Hypoxia, Brain, pubmed-meshheading:14678760-Male, pubmed-meshheading:14678760-Nerve Degeneration, pubmed-meshheading:14678760-Nerve Tissue Proteins, pubmed-meshheading:14678760-Phosphorylation, pubmed-meshheading:14678760-Protein-Serine-Threonine Kinases, pubmed-meshheading:14678760-Proto-Oncogene Proteins, pubmed-meshheading:14678760-Proto-Oncogene Proteins c-akt, pubmed-meshheading:14678760-Rats, pubmed-meshheading:14678760-Rats, Sprague-Dawley, pubmed-meshheading:14678760-Reaction Time, pubmed-meshheading:14678760-Signal Transduction, pubmed-meshheading:14678760-Sleep Apnea Syndromes, pubmed-meshheading:14678760-Time Factors, pubmed-meshheading:14678760-Transcription Factors
pubmed:year
2003
pubmed:articleTitle
Intermittent hypoxia induces time-dependent changes in the protein kinase B signaling pathway in the hippocampal CA1 region of the rat.
pubmed:affiliation
Kosair Children's Hospital Research Institute, Department of Pediatrics, University of Louisville, Louisville, KY 40202, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't