Movement Disorders (revue)

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Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement‐independent mechanism

Identifieur interne : 003736 ( Main/Exploration ); précédent : 003735; suivant : 003737

Serum from Sydenham's chorea patients modifies intracellular calcium levels in PC12 cells by a complement‐independent mechanism

Auteurs : Antonio L. Teixeira Jr [Brésil] ; Melissa M. Guimarães [Brésil] ; Marco Aurélio Romano-Silva [Brésil] ; Francisco Cardoso [Brésil]

Source :

RBID : ISTEX:F6E76324CDD028F50548213052BBA250789A1002

English descriptors

Abstract

The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody‐mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement‐inactivated serum from SC patients was associated with a significant increase in Ca2+ levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca2+ levels determined by SC patients sera correlated directly with the enzyme‐linked immunosorbent assay optical density values for anti–basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction. © 2005 Movement Disorder Society

Url:
DOI: 10.1002/mds.20418


Affiliations:


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Le document en format XML

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<term>Ca2+</term>
<term>Calcium (metabolism)</term>
<term>Child</term>
<term>Chorea (blood)</term>
<term>Chorea (immunology)</term>
<term>Complement System Proteins (pharmacology)</term>
<term>Enzyme-Linked Immunosorbent Assay (methods)</term>
<term>Female</term>
<term>Humans</term>
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<term>PC12 cells</term>
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<div type="abstract" xml:lang="en">The proposed pathogenesis of Sydenham's chorea (SC) is an autoantibody‐mediated basal ganglia dysfunction. Our study has shown that incubation of PC12 cells with complement‐inactivated serum from SC patients was associated with a significant increase in Ca2+ levels evoked by KCl stimulus (mean ± SEM, 341.0 ± 8.7% of fluorescence intensity, arbitrary units) when compared with incubation with control serum (313.8 ± 8.7% of fluorescence intensity, arbitrary units; P = 0.01). The increase in Ca2+ levels determined by SC patients sera correlated directly with the enzyme‐linked immunosorbent assay optical density values for anti–basal ganglia antibodies. Our study supports the hypothesis that antibodies against basal ganglia in SC may cause their dysfunction. © 2005 Movement Disorder Society</div>
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