Linked Life Data

16629625

Source:http://linkedlifedata.com/resource/pubmed/id/16629625

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3-4
pubmed:dateCreated
2006-4-24
pubmed:abstractText
Spinal cord scar tissue presents a combined physical and molecular barrier to axon regeneration. Theoretically, spinal cord injuries (SCIs) can be rendered more permissive to axon growth by either suppressing synthesis of misaligned, fibrotic scar tissue and associated axon growth inhibitors, or enzymatically degrading them. We have previously shown that acute infusion of human recombinant decorin core protein into discreet stab injuries of the rat dorsal column pathways effected a major suppression of inflammation, astrogliosis, and multiple axon growth inhibitory chondroitin sulfate proteoglycans, which combined to promote rapid axon growth across the injury site. The high efficiency of chondroitin sulfate proteoglycan (CSPG) core protein suppression (approximately 90%) suggested that decorin may promote CSPG degradation in addition to suppressing CSPG synthesis. As the serine protease plasmin can degrade axon growth inhibitory CSPGs (neurocan and phosphacan) and its zymogen, plasmininogen is synthesized by microglia, we have investigated whether decorin treatment of acute SCIs and cultured adult spinal cord microglia can increase plasminogen/ plasmin synthesis. Infusion of hr-decorin over the first 8 days post-SCI induced 10- and 17-fold increases in plasminogen and plasmin protein levels, respectively, within sites of injury and a threefold increase in microglial plasminogen mRNA in vitro. In addition to potentially degrading multiple axon growth inhibitory components of the glial scar, plasmin is known to play major roles in activating neurotrophins and promoting central nervous system (CNS) plasticity. The wider implications of decorin induction of plasmin in the injured spinal cord for axon regeneration, and recovery of function at acute and chronic time points post-SCI are reviewed.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0897-7151
pubmed:author
pubmed:issnType
Print
pubmed:volume
23
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
397-408
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16629625-Animals, pubmed-meshheading:16629625-Animals, Genetically Modified, pubmed-meshheading:16629625-Blotting, Western, pubmed-meshheading:16629625-Cicatrix, pubmed-meshheading:16629625-DNA, Complementary, pubmed-meshheading:16629625-Decorin, pubmed-meshheading:16629625-Extracellular Matrix Proteins, pubmed-meshheading:16629625-Female, pubmed-meshheading:16629625-Fibrinolysin, pubmed-meshheading:16629625-Mammary Glands, Animal, pubmed-meshheading:16629625-Mice, pubmed-meshheading:16629625-Microglia, pubmed-meshheading:16629625-Nerve Regeneration, pubmed-meshheading:16629625-Plasminogen, pubmed-meshheading:16629625-Proteoglycans, pubmed-meshheading:16629625-RNA, Messenger, pubmed-meshheading:16629625-Rats, pubmed-meshheading:16629625-Rats, Sprague-Dawley, pubmed-meshheading:16629625-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16629625-Spinal Cord Injuries
pubmed:articleTitle
Decorin promotes plasminogen/plasmin expression within acute spinal cord injuries and by adult microglia in vitro.
pubmed:affiliation
Department of Neurosurgery, Baylor College of Medicine, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't