BR Growth/differentiation factor-15 (GDF-15), a novel member of the TGF-beta superfamily, promotes survival of lesioned mesencephalic dopaminergic neurons in vitro and in vivo and is induced in neurons following cortical lesioning. Journal of Neural Transmission-Supplement

Typeset version

 

TY  - JOUR
  - Strelau, J.,Schober, A.,Sullivan, A.,Schilling, L.,Unsicker, K.
  - 2003
  - Unknown
  - Journal Of Neural Transmission-Supplement
  - BR Growth/differentiation factor-15 (GDF-15), a novel member of the TGF-beta superfamily, promotes survival of lesioned mesencephalic dopaminergic neurons in vitro and in vivo and is induced in neurons following cortical lesioning. Journal of Neural Transmission-Supplement
  - Validated
  - ()
  - 65
  - 197
  - 203
  - This review summarizes the evidence that GDF-15, a recently discovered member of the TGF-beta superfamily, is a trophic factor for nigral dopamine neurons, both in vitro and in vivo. Specifically, GDF-15 promotes survival and differentiation of embryonic rat dopaminergic neurons, but not of other neuron populations, with the exception of serotonergic raphe neurons. The neurotrophic effect of GDF-15 seems to be direct and not mediated through glial cells. In the rat 6-hydroxydopamine model of parkinsonism GDF-15 rescues intoxicated dopaminergic neurons and abolishes abnormal turning behavior. The most prominent site of synthesis of GDF-15 within the brain is the choroid plexus, which secretes GDF-15 into the cerebrospinal fluid, from where the molecule can penetrate through the ependymal layer into the parenchyma. Analysis of mouse mutants lacking GDF-15 will reveal whether the endogenous factor also has a role in promoting embryonic and protecting lesioned nigral dopamine neurons.
  - 0303-6995
  - ://000184862400013
DA  - 2003/NaN
ER  - 
@article{V18240431,
   = {Strelau,  J. and Schober,  A. and Sullivan,  A. and Schilling,  L. and Unsicker,  K. },
   = {2003},
   = {Unknown},
   = {Journal Of Neural Transmission-Supplement},
   = {BR Growth/differentiation factor-15 (GDF-15), a novel member of the TGF-beta superfamily, promotes survival of lesioned mesencephalic dopaminergic neurons in vitro and in vivo and is induced in neurons following cortical lesioning. Journal of Neural Transmission-Supplement},
   = {Validated},
   = {()},
   = {65},
  pages = {197--203},
   = {{This review summarizes the evidence that GDF-15, a recently discovered member of the TGF-beta superfamily, is a trophic factor for nigral dopamine neurons, both in vitro and in vivo. Specifically, GDF-15 promotes survival and differentiation of embryonic rat dopaminergic neurons, but not of other neuron populations, with the exception of serotonergic raphe neurons. The neurotrophic effect of GDF-15 seems to be direct and not mediated through glial cells. In the rat 6-hydroxydopamine model of parkinsonism GDF-15 rescues intoxicated dopaminergic neurons and abolishes abnormal turning behavior. The most prominent site of synthesis of GDF-15 within the brain is the choroid plexus, which secretes GDF-15 into the cerebrospinal fluid, from where the molecule can penetrate through the ependymal layer into the parenchyma. Analysis of mouse mutants lacking GDF-15 will reveal whether the endogenous factor also has a role in promoting embryonic and protecting lesioned nigral dopamine neurons.}},
  issn = {0303-6995},
   = {://000184862400013},
  source = {IRIS}
}
AUTHORSStrelau, J.,Schober, A.,Sullivan, A.,Schilling, L.,Unsicker, K.
YEAR2003
MONTHUnknown
JOURNAL_CODEJournal Of Neural Transmission-Supplement
TITLEBR Growth/differentiation factor-15 (GDF-15), a novel member of the TGF-beta superfamily, promotes survival of lesioned mesencephalic dopaminergic neurons in vitro and in vivo and is induced in neurons following cortical lesioning. Journal of Neural Transmission-Supplement
STATUSValidated
TIMES_CITED()
SEARCH_KEYWORD
VOLUME
ISSUE65
START_PAGE197
END_PAGE203
ABSTRACTThis review summarizes the evidence that GDF-15, a recently discovered member of the TGF-beta superfamily, is a trophic factor for nigral dopamine neurons, both in vitro and in vivo. Specifically, GDF-15 promotes survival and differentiation of embryonic rat dopaminergic neurons, but not of other neuron populations, with the exception of serotonergic raphe neurons. The neurotrophic effect of GDF-15 seems to be direct and not mediated through glial cells. In the rat 6-hydroxydopamine model of parkinsonism GDF-15 rescues intoxicated dopaminergic neurons and abolishes abnormal turning behavior. The most prominent site of synthesis of GDF-15 within the brain is the choroid plexus, which secretes GDF-15 into the cerebrospinal fluid, from where the molecule can penetrate through the ependymal layer into the parenchyma. Analysis of mouse mutants lacking GDF-15 will reveal whether the endogenous factor also has a role in promoting embryonic and protecting lesioned nigral dopamine neurons.
PUBLISHER_LOCATION
ISBN_ISSN0303-6995
EDITION
URL://000184862400013
DOI_LINK
FUNDING_BODY
GRANT_DETAILS