ParkinsonFranceV1, Main, Exploration, bibRecord, 002D49

Proliferation of microglial cells induced by 1-methyl-4-phenylpyridinium in mesencephalic cultures results from an astrocyte-dependent mechanism : role of granulocyte macrophage colony-stimulating factor

Identifieur interne : 002D49 ( Main/Exploration ); précédent : 002D48; suivant : 002D50

Proliferation of microglial cells induced by 1-methyl-4-phenylpyridinium in mesencephalic cultures results from an astrocyte-dependent mechanism : role of granulocyte macrophage colony-stimulating factor

Auteurs : Carmen Henze [France] ; Andreas Hartmann [France] ; Thomas Lescot [France] ; Etienne C. Hirsch [France] ; Patrick P. Michel [France]

Source :

Journal of neurochemistry [ 0022-3042 ] ; 2005.

RBID : Pascal:06-0019861

Descripteurs français

Pascal (Inist)
- Multiplication cellulaire, Astrocyte, Facteur stimulant colonie granulocyte macrophage, Physiopathologie, Mort cellulaire, Modèle animal, In vitro, Neurotoxine, Parkinson maladie, Survie, Culture cellulaire, Traitement.

English descriptors

KwdEn :
- Animal model, Astrocyte, Cell culture, Cell death, Cell proliferation, Granulocyte macrophage colony stimulating factor, In vitro, Neurotoxin, Parkinson disease, Pathophysiology, Survival, Treatment.

Abstract

There is evidence that an inflammatory microglial reaction participates in the pathophysiology of dopaminergic neuronal death in Parkinson's disease and in animal models of the disease. However, this phenomenon remains incompletely characterized. Using an in vitro model of neuronal/ glial mesencephalic cultures, we show that the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP⁺) stimulates the proliferation of microglial cells at concentrations that selectively reduce the survival of DA neurones. The mitogenic action of MPP⁺ was not the mere consequence of neuronal cell demise as the toxin produced the same effect in a model system of neuronal/glial cortical cultures, where target DA neurones are absent. Consistent with this observation, the proliferative effect of MPP⁺ was also detectable in neurone-free microglial/astroglial cultures. It disappeared, however, when MPP⁺ was added to pure microglial cell cultures suggesting that astrocytes played a key role in the mitogenic mechanism. Accordingly, the proliferation of microglial cells in response to MPP⁺ treatment was mimicked by granulocyte macrophage colony-stimulating factor (GM-CSF), a proinflammatory cytokine produced by astrocytes and was blocked by a neutralizing antibody to GM-CSF. Thus, we conclude that the microglial reaction observed following MPP⁺ exposure depends on astrocytic factors, e.g. GM-CSF, a finding that may have therapeutic implications.

Affiliations:

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Le document en format XML

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<front><div type="abstract" xml:lang="en">There is evidence that an inflammatory microglial reaction participates in the pathophysiology of dopaminergic neuronal death in Parkinson's disease and in animal models of the disease. However, this phenomenon remains incompletely characterized. Using an in vitro model of neuronal/ glial mesencephalic cultures, we show that the dopaminergic neurotoxin 1-methyl-4-phenylpyridinium (MPP<sup>+</sup>
) stimulates the proliferation of microglial cells at concentrations that selectively reduce the survival of DA neurones. The mitogenic action of MPP<sup>+</sup>
 was not the mere consequence of neuronal cell demise as the toxin produced the same effect in a model system of neuronal/glial cortical cultures, where target DA neurones are absent. Consistent with this observation, the proliferative effect of MPP<sup>+</sup>
 was also detectable in neurone-free microglial/astroglial cultures. It disappeared, however, when MPP<sup>+</sup>
 was added to pure microglial cell cultures suggesting that astrocytes played a key role in the mitogenic mechanism. Accordingly, the proliferation of microglial cells in response to MPP<sup>+</sup>
 treatment was mimicked by granulocyte macrophage colony-stimulating factor (GM-CSF), a proinflammatory cytokine produced by astrocytes and was blocked by a neutralizing antibody to GM-CSF. Thus, we conclude that the microglial reaction observed following MPP<sup>+</sup>
 exposure depends on astrocytic factors, e.g. GM-CSF, a finding that may have therapeutic implications.</div>
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Proliferation of microglial cells induced by 1-methyl-4-phenylpyridinium in mesencephalic cultures results from an astrocyte-dependent mechanism : role of granulocyte macrophage colony-stimulating factor

Proliferation of microglial cells induced by 1-methyl-4-phenylpyridinium in mesencephalic cultures results from an astrocyte-dependent mechanism : role of granulocyte macrophage colony-stimulating factor

Source :

Descripteurs français

English descriptors

Abstract

Links toward previous steps (curation, corpus...)

Le document en format XML

Pour manipuler ce document sous Unix (Dilib)

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