Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-8-26
pubmed:abstractText
Elevation of intracellular heat shock protein (Hsp)70 increases resistance of cells to many physical and metabolic insults. We tested the hypothesis that treatment with Hsc70 can also produce that effect, using the model of axotomy-induced neuronal death in the neonatal mouse. The sciatic nerve was sectioned and in some animals purified bovine brain Hsc70 was applied to the proximal end of the nerve immediately thereafter and again 3 days later. Seven days postaxotomy, the surviving sensory neurons of the lumbar dorsal root ganglion (DRG) and motoneurons of the lumbar ventral spinal cord were counted to assess cell death. Axotomy induced the death of approximately 33% of DRG neurons and 50% of motoneurons, when examined 7 days postinjury. Application of exogenous Hsc70 prevented axotomy-induced death of virtually all sensory neurons, but did not significantly alter motoneuron death. Thus, Hsc70 may prove to be useful in the repair of peripheral sensory nerve damage.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
1355-8145
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
161-6
pubmed:dateRevised
2008-11-20
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Exogenous heat shock cognate protein Hsc 70 prevents axotomy-induced death of spinal sensory neurons.
pubmed:affiliation
Department of Neurobiology & Anatomy, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, NC 27157-1010, USA. lhouenou@bgsm.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't