Open AccessQuantification of Neurotrophin mRNA Expression in PMN Mouse: Modulation by Xaliproden
Author(s) -
Aline Appert-Collin,
François H.T. Duong,
Patricia PassillyDegrace,
J.-P. Gies,
JeanMarie Warter,
Philippe Poindron
Publication year - 2004
Publication title -
international journal of immunopathology and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.724
H-Index - 53
eISSN - 2058-7384
pISSN - 0394-6320
DOI - 10.1177/039463200401700207
Subject(s) - neurotrophin , trk receptor , in vivo , amyotrophic lateral sclerosis , messenger rna , neurotrophic factors , in vitro , reverse transcription polymerase chain reaction , biology , neurotrophin 3 , microbiology and biotechnology , brain derived neurotrophic factor , medicine , receptor , biochemistry , gene , genetics , disease
Compounds possessing neurotrophic properties may represent a possible treatment for neurodegenerative disorders such as amyotrophic lateral sclerosis. Xaliproden (SR57746A), an orally-active non-peptide compound, which has been found to exhibit neurotrophic effects in vitro and in vivo, increase the lifespan and delay the progression of motor neuron degeneration in PMN mice. We have used a quantitative reverse transcription/polymerase chain reaction amplification technique to study the regulation of neurotrophin mRNA and trk mRNA expression in PMN mice. NGF and NT-3 mRNA are downregulated in PMN mice. These deficiencies can be overcome by treatment with xaliproden. Such an effect could contribute to neurotrophic effects of xaliproden in vivo and in vitro.
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