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Modulation of acetylcholine receptor expression in seronegative myasthenia gravis

2000; Wiley; Volume: 48; Issue: 5 Linguagem: Inglês

10.1002/1531-8249(200011)48

1531-8249

Sandrine Poëa, Thierry Guyon, Jocelyne Bidault, Corinne Bruand, Vincent Mouly, Sonia Berrih‐Aknin,

Coagulation, Bradykinin, Polyphosphates, and Angioedema

Annals of NeurologyVolume 48, Issue 5 p. 696-705 Original Article Modulation of acetylcholine receptor expression in seronegative myasthenia gravis Sandrine Poea PhD, Sandrine Poea PhD CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceSearch for more papers by this authorThierry Guyon PhD, Thierry Guyon PhD Institut de Recherche Jouveinal/Parke-Davis, Fresnes, FranceSearch for more papers by this authorJocelyne Bidault MSc, Jocelyne Bidault MSc CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceSearch for more papers by this authorCorinne Bruand MSc, Corinne Bruand MSc CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceSearch for more papers by this authorVincent Mouly PhD, Vincent Mouly PhD CNRS UMR 7000, Faculté de Médecine Pitié-Salpétrière, Paris, FranceSearch for more papers by this authorSonia Berrih-Aknin PhD, Corresponding Author Sonia Berrih-Aknin PhD CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceLaboratoire de Physiologie Thymique, CNRS ESA 8078, Hôpital Marie Lannelongue, 133 Avenue de la Résistance, 92350 Le Plessis-Robinson, FranceSearch for more papers by this author Sandrine Poea PhD, Sandrine Poea PhD CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceSearch for more papers by this authorThierry Guyon PhD, Thierry Guyon PhD Institut de Recherche Jouveinal/Parke-Davis, Fresnes, FranceSearch for more papers by this authorJocelyne Bidault MSc, Jocelyne Bidault MSc CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceSearch for more papers by this authorCorinne Bruand MSc, Corinne Bruand MSc CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceSearch for more papers by this authorVincent Mouly PhD, Vincent Mouly PhD CNRS UMR 7000, Faculté de Médecine Pitié-Salpétrière, Paris, FranceSearch for more papers by this authorSonia Berrih-Aknin PhD, Corresponding Author Sonia Berrih-Aknin PhD CNRS ESA 8078, Hôpital Marie Lannelongue, Le Plessis-Robinson, FranceLaboratoire de Physiologie Thymique, CNRS ESA 8078, Hôpital Marie Lannelongue, 133 Avenue de la Résistance, 92350 Le Plessis-Robinson, FranceSearch for more papers by this author First published: 04 April 2001 https://doi.org/10.1002/1531-8249(200011)48:5 3.0.CO;2-SCitations: 9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Abstract In a previous study, we demonstrated a compensatory mechanism for regulating acetylcholine receptor (AChR) gene expression in muscle biopsies from seropositive and seronegative (SN) myasthenia gravis (MG) patients. To further characterize the AChR regulation mechanisms involved in SNMG disease, we investigated the effects of MG sera on nicotinic AChR expression (at the protein and messenger RNA [mRNA] levels) in cultured human muscle cells. Sera from SNMG patients induced an in vitro increase in the level of nicotinic AChR β-subunit mRNA but did not cause a decrease in AChR protein level. This apparent discrepancy was not due to a higher level of AChR synthesis as demonstrated by analysis of AChR turnover. In SN patients, the increase in β-subunit mRNA level was followed after 48 hours by a slight increase in the amount of AChR surface protein. This regulation of nicotinic receptor expression was due to the purified IgG-containing fraction. Thus, sera from SNMG patients contain an immunoglobulin that induces an increase in AChR mRNA without causing a decrease in AChR protein level, suggesting an indirect regulatory mechanism involving another surface molecule. This model is therefore useful for defining the targets involved in the pathogenesis of SNMG disease. Ann Neurol 2000;48:696–705 Citing Literature Volume48, Issue5November 2000Pages 696-705 RelatedInformation