Linked Life Data

12882321

Source:http://linkedlifedata.com/resource/pubmed/id/12882321

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-7-28
pubmed:abstractText
Physiological and pathological aging of the central nervous system (CNS) is characterized by functional neuronal impairments which may lead to perturbed cell homeostasis and eventually to neuronal death. Many toxic events may underlie age-related neurodegeneration. These include the effects of beta amyloid, Tau and mutated presenilin proteins, free radicals and oxidative stress, pro-inflammatory cytokines and lack of growth factor support, which can be individually or collectively involved. Taken individually, these toxicants can induce very diverse cell responses, thus requiring individually targeted corrective interventions upstream of common cell death (apoptotic) pathways. Recent preliminary evidence suggests that the pro-inflammatory cytokine tumour necrosis factor alpha (TNFalpha) and growth factor withdrawal can both activate a common apoptotic pathway in nerve growth factor (NGF)-responsive PC12 cells involving caspase 3, albeit through very distinct upstream pathways: the former through active signalling and the latter through passive or lack of survival signalling. Here, we show that NGF can rescue PC12 cells from both growth factor withdrawal- and TNFalpha-promoted cell death. However, NGF rescue from growth factor withdrawal requires NGF signalling through the high-affinity tyrosine kinase receptor (TrkA), while NGF rescue from TNFalpha-promoted cell death requires NGF signalling through the low-affinity p75NTR receptor. These results strengthen the idea that prevention of age- or pathology-associated neurodegeneration may require varied molecular approaches reflecting the diversity of the toxicants involved, possibly acting simultaneously.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1474-9718
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
83-92
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12882321-Animals, pubmed-meshheading:12882321-Apoptosis, pubmed-meshheading:12882321-Culture Media, pubmed-meshheading:12882321-Dose-Response Relationship, Drug, pubmed-meshheading:12882321-Humans, pubmed-meshheading:12882321-Neoplasm Proteins, pubmed-meshheading:12882321-Nerve Growth Factor, pubmed-meshheading:12882321-Neurites, pubmed-meshheading:12882321-PC12 Cells, pubmed-meshheading:12882321-Phosphorylation, pubmed-meshheading:12882321-Protein Processing, Post-Translational, pubmed-meshheading:12882321-Rats, pubmed-meshheading:12882321-Receptor, Nerve Growth Factor, pubmed-meshheading:12882321-Receptor, trkA, pubmed-meshheading:12882321-Receptors, Nerve Growth Factor, pubmed-meshheading:12882321-Signal Transduction, pubmed-meshheading:12882321-Tumor Necrosis Factor-alpha
pubmed:year
2003
pubmed:articleTitle
Tumour necrosis factor-alpha- vs. growth factor deprivation-promoted cell death: different receptor requirements for mediating nerve growth factor-promoted rescue.
pubmed:affiliation
Center for Biomedical Engineering, The University of Texas Medical Branch at Galveston, Galveston, TX 77555 -1043, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't