Source:http://linkedlifedata.com/resource/pubmed/id/17379257
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
24-25
|
| pubmed:dateCreated |
2007-6-4
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| pubmed:abstractText |
The cholinergic control over inflammatory reactions calls for deciphering the corresponding protein partners. An example is blood-nerve barrier disruption allowing penetration of inflammatory factors, which is notably involved in various neuropathies due to yet unknown molecular mechanism(s). In rats, lipopolysaccharide (LPS) administration followed by intra-neural (i.n.) saline injection inducing a focal blood-nerve disruption leads to systemic inflammatory reaction accompanied by transient conduction impairment in the sciatic nerve. Here, we provide evidence compatible with the hypothesis that ARP, the naturally cleavable C-terminal peptide of the stress-induced "readthrough" acetylcholinesterase variant (AChE-R), is causally involved in the emergence of this LPS-induced conduction impairment. Intra-neural injection to naïve rats of conditioned medium from cultured splenocytes exposed to LPS in vitro (reactive splenocyte medium) induced a transient conduction impairment that was accompanied by facilitated accumulation of cleaved intra-neural ARP. Protein kinase C (PKC) betaII, known to interact with ARP, was significantly elevated in the LPS-exposed sciatic nerve preparations. Moreover, direct i.n. injection of synthetic ARP30, bearing the mouse AChE-R C-terminal sequence, similarly induced PKCbetaII expression and conduction impairment. The induction of neural conduction impairment by ARP, possibly through its interaction with PKCbetaII, suggests a role for AChE-R expression in inflammation-associated neuropathies.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholine,
http://linkedlifedata.com/resource/pubmed/chemical/Acetylcholinesterase,
http://linkedlifedata.com/resource/pubmed/chemical/Culture Media, Conditioned,
http://linkedlifedata.com/resource/pubmed/chemical/Lipopolysaccharides,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Cholinergic
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| pubmed:status |
MEDLINE
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| pubmed:month |
May
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| pubmed:issn |
0024-3205
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
30
|
| pubmed:volume |
80
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2369-74
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| pubmed:meshHeading |
pubmed-meshheading:17379257-Acetylcholine,
pubmed-meshheading:17379257-Acetylcholinesterase,
pubmed-meshheading:17379257-Action Potentials,
pubmed-meshheading:17379257-Amino Acid Sequence,
pubmed-meshheading:17379257-Animals,
pubmed-meshheading:17379257-Catalysis,
pubmed-meshheading:17379257-Cells, Cultured,
pubmed-meshheading:17379257-Culture Media, Conditioned,
pubmed-meshheading:17379257-Female,
pubmed-meshheading:17379257-Immunoblotting,
pubmed-meshheading:17379257-Inflammation,
pubmed-meshheading:17379257-Lipopolysaccharides,
pubmed-meshheading:17379257-Models, Biological,
pubmed-meshheading:17379257-Molecular Sequence Data,
pubmed-meshheading:17379257-Muscles,
pubmed-meshheading:17379257-Peptide Fragments,
pubmed-meshheading:17379257-Peripheral Nervous System Diseases,
pubmed-meshheading:17379257-Rats,
pubmed-meshheading:17379257-Rats, Inbred Lew,
pubmed-meshheading:17379257-Receptors, Cholinergic,
pubmed-meshheading:17379257-Sciatic Nerve,
pubmed-meshheading:17379257-Spleen
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| pubmed:year |
2007
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| pubmed:articleTitle |
Readthrough acetylcholinesterase in inflammation-associated neuropathies.
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| pubmed:affiliation |
Department of Neurology, The Joseph Sagol Neuroscience Center, Chaim Sheba Medical Center, Tel-Hashomer 52621, Israel.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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