Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
26
pubmed:dateCreated
2009-12-17
pubmed:abstractText
STUDY DESIGN.: To examine the distribution of apoptotic cells and expression of tumor necrosis factor (TNF)-alpha and its receptors in the spinal hyperostotic mouse (twy/twy) with chronic cord compression using immunohistochemical methods. OBJECTIVE.: To study the mechanisms of apoptosis, particularly in oligodendrocytes, which could contribute to degenerative change and demyelination in chronic mechanical cord compression. SUMMARY OF BACKGROUND DATA.: TNF-alpha acts as an external signal initiating apoptosis in neurons and oligodendrocytes after spinal cord injury. Chronic spinal cord compression caused neuronal loss, myelin destruction, and axonal degeneration. However, the biologic mechanisms of apoptosis in chronically compressed spinal cord remain unclear. METHODS.: The cervical spinal cord of 34 twy mice aged 20 to 24 weeks and 11 control animals were examined. The apoptotic cells were detected by the terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL) staining. The expression and the localization of TNF-alpha, TNF receptor 1 (TNFR1), and TNF receptor 2 (TNFR2) were examined using immunoblot and immnohistochemical analysis. RESULTS.: The number of TUNEL-positive cells in the white matter increased with the severity of compression, which was further increased bilaterally in the white matter of twy/twy mice. Double immunofluorescence staining showed that the number of cells positive for TUNEL and RIP, a marker of oligodendrocytes, increased in the white matter with increased severity of cord compression. Immunoblot analysis demonstrated overexpression of TNF-alpha, TNFR1, and TNFR2 in severe compression. The expression of TNF-alpha appeared in local cells including microglia while that of TNFR1 and TNFR2 was noted in apoptotic oligodendrocytes. CONCLUSION.: Our results suggested that the proportion of apoptotic oligodendrocytes, causing spongy axonal degeneration and demyelination, correlated with the magnitude of cord compression and that overexpression of TNF-alpha, TNFR1, and TNFR2 seems to participate in apoptosis of such cells in the chronically compressed spinal cord.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
1528-1159
pubmed:author
pubmed:issnType
Electronic
pubmed:day
15
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2848-57
pubmed:meshHeading
pubmed-meshheading:19949368-Animals, pubmed-meshheading:19949368-Apoptosis, pubmed-meshheading:19949368-Blotting, Western, pubmed-meshheading:19949368-Cell Count, pubmed-meshheading:19949368-Cervical Vertebrae, pubmed-meshheading:19949368-Chronic Disease, pubmed-meshheading:19949368-Fluorescent Antibody Technique, pubmed-meshheading:19949368-Hyperostosis, pubmed-meshheading:19949368-In Situ Nick-End Labeling, pubmed-meshheading:19949368-Mice, pubmed-meshheading:19949368-Mice, Transgenic, pubmed-meshheading:19949368-Microscopy, Electron, Transmission, pubmed-meshheading:19949368-Microscopy, Fluorescence, pubmed-meshheading:19949368-Nerve Degeneration, pubmed-meshheading:19949368-Neurons, pubmed-meshheading:19949368-Oligodendroglia, pubmed-meshheading:19949368-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:19949368-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:19949368-Severity of Illness Index, pubmed-meshheading:19949368-Spinal Cord, pubmed-meshheading:19949368-Spinal Cord Compression, pubmed-meshheading:19949368-Statistics, Nonparametric, pubmed-meshheading:19949368-Stress, Mechanical, pubmed-meshheading:19949368-Tumor Necrosis Factor-alpha
pubmed:year
2009
pubmed:articleTitle
Tumor necrosis factor-alpha and its receptors contribute to apoptosis of oligodendrocytes in the spinal cord of spinal hyperostotic mouse (twy/twy) sustaining chronic mechanical compression.
pubmed:affiliation
Department of Orthopaedics and Rehabilitation Medicine, The University of Fukui, Fukui, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't