Linked Life Data

17996195

Source:http://linkedlifedata.com/resource/pubmed/id/17996195

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-11-26
pubmed:abstractText
Expression of the pro-inflammatory cytokine interleukin-1 beta (IL-1beta) is increased following the nervous system injury. Generally IL-1beta induces inflammation, leading to neural degeneration, while several neuropoietic effects have also been reported. Although neurite outgrowth is an important step in nerve regeneration, whether IL-1beta takes advantages on it is unclear. Now we examine how it affects neurite outgrowth. Following sciatic nerve injury, expression of IL-1beta is increased in Schwann cells around the site of injury, peaking 1 day after injury. In dorsal root ganglion (DRG) neurons and cerebellar granule neurons (CGNs), neurite outgrowth is inhibited by the addition of myelin-associated glycoprotein (MAG), activating RhoA. IL-1beta overcomes MAG-induced neurite outgrowth inhibition, by deactivating RhoA. Intracellular signaling experiments reveal that p38 MAPK, and not nuclear factor-kappa B (NF-kappaB), mediated this effect. These findings suggest that IL-1beta may contribute to nerve regeneration by promoting neurite outgrowth following nerve injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1090-2104
pubmed:author
pubmed:issnType
Electronic
pubmed:day
11
pubmed:volume
365
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
375-80
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
IL-1beta promotes neurite outgrowth by deactivating RhoA via p38 MAPK pathway.
pubmed:affiliation
Department of Orthopaedics, Osaka University Graduate School of Medicine, Suita, Osaka 565-0871, Japan.
pubmed:publicationType
Journal Article