Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2002-3-28
pubmed:abstractText
Although cytokine-induced nuclear factor kappaB (NF-kappaB) pathways are involved in muscle wasting subsequent to disease, their potential role in disuse muscle atrophy has not been characterized. Seven days of hind limb unloading led to a 10-fold activation of an NF-kappaB-dependent reporter in rat soleus muscle but not the atrophy-resistant extensor digitorum longus muscle. Nuclear levels of p50 were markedly up-regulated, c-Rel was moderately up-regulated, Rel B was down-regulated, and p52 and p65 were unchanged in unloaded solei. The nuclear IkappaB protein Bcl-3 was increased. There was increased binding to an NF-kappaB consensus oligonucleotide, and this complex bound antibodies to p50, c-Rel, and Bcl-3 but not other NF-kappaB family members. Tumor necrosis factor alpha (TNF-alpha) and TNF receptor-associated factor 2 protein were moderately down-regulated. There was no difference in p38, c-Jun NH(2)-terminal kinase or Akt activity, nor were activator protein 1 or nuclear factor of activated T cell-dependent reporters activated. Thus, whereas several NF-kappaB family members are up-regulated, the prototypical markers of cytokine-induced activation of NF-kappaB seen with disease-related wasting are not evident during disuse atrophy. Levels of an anti-apoptotic NF-kappaB target, Bcl-2, were increased fourfold whereas proapoptotic proteins Bax and Bak decreased. The evidence presented here suggests that disuse muscle atrophy is associated with activation of an alternative NF-kappaB pathway that involves the activation of p50 but not p65.
pubmed:grant
pubmed:keyword
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1530-6860
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
529-38
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11919155-Animals, pubmed-meshheading:11919155-Cell Nucleus, pubmed-meshheading:11919155-Consensus Sequence, pubmed-meshheading:11919155-Electrophoretic Mobility Shift Assay, pubmed-meshheading:11919155-Female, pubmed-meshheading:11919155-Genes, Reporter, pubmed-meshheading:11919155-Hindlimb Suspension, pubmed-meshheading:11919155-I-kappa B Kinase, pubmed-meshheading:11919155-Models, Biological, pubmed-meshheading:11919155-Muscle, Skeletal, pubmed-meshheading:11919155-Muscular Atrophy, pubmed-meshheading:11919155-NF-kappa B, pubmed-meshheading:11919155-NF-kappa B p50 Subunit, pubmed-meshheading:11919155-Protein-Serine-Threonine Kinases, pubmed-meshheading:11919155-Proto-Oncogene Proteins, pubmed-meshheading:11919155-Proto-Oncogene Proteins c-bcl-2, pubmed-meshheading:11919155-Rats, pubmed-meshheading:11919155-Signal Transduction, pubmed-meshheading:11919155-Transcription Factors, pubmed-meshheading:11919155-Tumor Necrosis Factor-alpha
pubmed:year
2002
pubmed:articleTitle
Activation of an alternative NF-kappaB pathway in skeletal muscle during disuse atrophy.
pubmed:affiliation
Boston University, Department of Health Sciences, Boston, Massachusetts 02215, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't