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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2005-1-31
pubmed:abstractText
The causative pathomechanism of sporadic amyotrophic lateral sclerosis (ALS) is not clearly understood. Using microarray technology combined with laser-captured microdissection, gene expression profiles of degenerating spinal motor neurons isolated from autopsied patients with sporadic ALS were examined. Gene expression was quantitatively assessed by real-time reverse transcription polymerase chain reaction and in situ hybridization. Spinal motor neurons showed a distinct gene expression profile from the whole spinal ventral horn. Three percent of genes examined were downregulated, and 1% were upregulated in motor neurons. Downregulated genes included those associated with cytoskeleton/axonal transport, transcription, and cell surface antigens/receptors, such as dynactin, microtubule-associated proteins, and early growth response 3 (EGR3). In contrast, cell death-associated genes were mostly upregulated. Promoters for cell death pathway, death receptor 5, cyclins A1 and C, and caspases-1, -3, and -9, were upregulated, whereas cell death inhibitors, acetyl-CoA transporter, and NF-kappaB were also upregulated. Moreover, neuroprotective neurotrophic factors such as ciliary neurotrophic factor (CNTF), Hepatocyte growth factor (HGF), and glial cell line-derived neurotrophic factor were upregulated. Inflammation-related genes, such as those belonging to the cytokine family, were not, however, significantly upregulated in either motor neurons or ventral horns. The motor neuron-specific gene expression profile in sporadic ALS can provide direct information on the genes leading to neurodegeneration and neuronal death and are helpful for developing new therapeutic strategies.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0364-5134
pubmed:author
pubmed:issnType
Print
pubmed:volume
57
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
236-51
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15668976-Adult, pubmed-meshheading:15668976-Aged, pubmed-meshheading:15668976-Aged, 80 and over, pubmed-meshheading:15668976-Amyotrophic Lateral Sclerosis, pubmed-meshheading:15668976-Anterior Horn Cells, pubmed-meshheading:15668976-DNA Primers, pubmed-meshheading:15668976-Female, pubmed-meshheading:15668976-Gene Expression Profiling, pubmed-meshheading:15668976-Humans, pubmed-meshheading:15668976-Immunohistochemistry, pubmed-meshheading:15668976-In Situ Hybridization, pubmed-meshheading:15668976-Lasers, pubmed-meshheading:15668976-Male, pubmed-meshheading:15668976-Microdissection, pubmed-meshheading:15668976-Middle Aged, pubmed-meshheading:15668976-Motor Neurons, pubmed-meshheading:15668976-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:15668976-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:15668976-Spinal Cord
pubmed:year
2005
pubmed:articleTitle
Gene expression profile of spinal motor neurons in sporadic amyotrophic lateral sclerosis.
pubmed:affiliation
Department of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Japan.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't