Linked Life Data

15880494

Source:http://linkedlifedata.com/resource/pubmed/id/15880494

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-5-11
pubmed:abstractText
Inhibition of the small GTPase ras homology protein (Rho) or its downstream target, the Rho-associated kinase (ROCK), has been shown to promote axon regeneration and to improve functional recovery following spinal cord injury (SCI) in the adult rat. Here, we have analyzed the expression of RhoA and RhoB following spinal cord injury in order to assess whether Rho is a possible target for late pharmacological intervention. In control spinal cords, RhoA(+) cells were almost absent, whereas RhoB was localized to some ependymal cells, a few microglia, and some dissociated neurons. In injured spinal cords, RhoA(+) and RhoB(+)cells accumulated at perilesional areas and in the developing necrotic core early after injury at day 1. After reaching their maximum levels (RhoA at day 3; RhoB at day 1), RhoA(+) and RhoB(+) cell numbers remained significantly elevated until day 28. In areas remote from the lesion (> or =0.75 mm), a more discrete accumulation of RhoA(+) and RhoB(+) cells was observed, primarily in areas of ongoing Wallerian degeneration. RhoA and RhoB were predominantly expressed by polymorphonuclear granulocytes, ED1(+) microglia/macrophages, oligodendrocytes, some neurons, and swollen axons/neurites. Furthermore, expression was located to lesional, reactive astrocytes and fibroblastoid cells confined to areas of scar formation. Our experiments have determined that most RhoA(+) and RhoB(+) cells (>70%) are of mononuclear origin. The persistent presence of lesional RhoA(+) and RhoB(+) axon/neurite fibers over a period of 4 weeks after injury suggests that Rho inhibition is a putative therapeutic concept also for delayed intervention after SCI.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9967
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
487
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
166-75
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15880494-Amyloid beta-Protein Precursor, pubmed-meshheading:15880494-Animals, pubmed-meshheading:15880494-Brain, pubmed-meshheading:15880494-Cell Count, pubmed-meshheading:15880494-Cyclooxygenase 2, pubmed-meshheading:15880494-Ectodysplasins, pubmed-meshheading:15880494-Gene Expression Regulation, pubmed-meshheading:15880494-Glial Fibrillary Acidic Protein, pubmed-meshheading:15880494-Immunohistochemistry, pubmed-meshheading:15880494-Lymphocytes, pubmed-meshheading:15880494-Male, pubmed-meshheading:15880494-Membrane Proteins, pubmed-meshheading:15880494-Myelin Basic Proteins, pubmed-meshheading:15880494-Prostaglandin-Endoperoxide Synthases, pubmed-meshheading:15880494-Rats, pubmed-meshheading:15880494-Rats, Inbred Lew, pubmed-meshheading:15880494-Spinal Cord Injuries, pubmed-meshheading:15880494-Time Factors, pubmed-meshheading:15880494-rhoA GTP-Binding Protein, pubmed-meshheading:15880494-rhoB GTP-Binding Protein
pubmed:year
2005
pubmed:articleTitle
Prolonged lesional expression of RhoA and RhoB following spinal cord injury.
pubmed:affiliation
Institute of Brain Research, D-72076 Tuebingen, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't