Lithium facilitates apoptotic signaling induced by activation of the Fas death domain-containing receptor View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2004-05-24

AUTHORS

Ling Song, Tong Zhou, Richard S Jope

ABSTRACT

BackgroundLithium, a mood stabilizer widely used to treat bipolar disorder, also is a neuroprotectant, providing neurons protection from apoptosis induced by a broad spectrum of toxic conditions. A portion of this neuroprotection is due to lithium's inhibition of glycogen synthase kinase-3. The present investigation examined if the neuroprotection provided by lithium included apoptosis induced by stimulation of the death domain-containing receptor Fas.ResultsInstead of providing protection, treatment with 20 mM lithium significantly increased apoptotic signaling induced by activation of Fas, and this occurred in both Jurkat cells and differentiated immortalized hippocampal neurons. Other inhibitors of glycogen synthase kinase-3, including 20 μM indirubin-3'-monoxime, 5 μM kenpaullone, and 5 μM rottlerin, also facilitated Fas-induced apoptotic signaling, indicating that the facilitation of apoptosis by lithium was due to inhibition of glycogen synthase kinase-3.ConclusionsThese results demonstrate that lithium is not always a neuroprotectant, and it has the opposite effect of facilitating apoptosis mediated by stimulation of death domain-containing receptors. More... »

PAGES

20

Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/1471-2202-5-20

DOI

http://dx.doi.org/10.1186/1471-2202-5-20

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1036629659

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/15157283


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