Article

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

Movement Disorders Clinic, Hospital das Clínicas, Universidade Federal de Minas Gerais, Belo Horizonte, Brazil.
Movement Disorders (impact factor: 4.51). 08/2005; 20(7):843-5. DOI:10.1002/mds.20418 pp.843-5
Source: PubMed

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.

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Keywords

Ca2+ levels
 
Ca2+ levels evoked
 
enzyme-linked immunosorbent assay optical density values
 
fluorescence intensity
 
incubation
 
KCl stimulus
 
PC12 cells
 
proposed pathogenesis
 
SC
 
SC patients
 
SC patients sera correlated