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Induction of interleukin-6 by depolarization of neurons

Interleukin-6 (IL-6) has neuromodulatory and neuroprotective effects in vivo. It is expressed in glial cells and neurons both under physiological conditions and in various neurological diseases. Although the expression of IL-6 in glia has been intensely investigated, little is known about the regula...

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Main Authors: Sallmann, Svea (Author) , Jüttler, Eric (Author) , Prinz, Simone (Author) , Petersen, Nicole (Author) , Knopf, Udo (Author) , Weiser, Thomas (Author) , Schwaninger, Markus (Author)
Format: Article (Journal)
Language:English
Published: December 1, 2000
In: The journal of neuroscience
Year: 2000, Volume: 20, Issue: 23, Pages: 8637-8642
ISSN:1529-2401
DOI:10.1523/JNEUROSCI.20-23-08637.2000
Online Access:Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1523/JNEUROSCI.20-23-08637.2000
Verlag, lizenzpflichtig, Volltext: https://www.jneurosci.org/content/20/23/8637
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Author Notes:Svea Sallmann, Eric Jüttler, Simone Prinz, Nicole Petersen, Udo Knopf, Thomas Weiser, and Markus Schwaninger

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520 |a Interleukin-6 (IL-6) has neuromodulatory and neuroprotective effects in vivo. It is expressed in glial cells and neurons both under physiological conditions and in various neurological diseases. Although the expression of IL-6 in glia has been intensely investigated, little is known about the regulation of IL-6 production by neurons. Therefore, we investigated the regulation of IL-6 expression in neurons. Membrane depolarization raised IL-6 mRNA accumulation in primary cortical cells and the PC-12 cell line.In vivo, IL-6 mRNA in the brain increased significantly after epileptic seizures. To investigate IL-6 gene transcription, PC-12 cells were transfected with reporter gene constructs containing the human IL-6 promoter. Membrane depolarization raised IL-6 transcription twofold to fourfold. This increase could be blocked by lowering extracellular Ca2+ levels or by inhibiting L-type Ca2+ channels or Ca2+/calmodulin-dependent protein kinases. Internal mutations in various elements of the IL-6 promoter revealed the glucocorticoid response element (GRE) 2 to be a depolarization-responsive element. Although the GRE2 bound the glucocorticoid receptor (GR) and was stimulated by dexamethasone, the GR was not responsible for the effect of membrane depolarization because a consensus GRE did not mediate stimulation by membrane depolarization. Instead, another yet undefined factor that binds to the IL-6 GRE2 may mediate the response to membrane depolarization. These data demonstrate that the expression of IL-6 in neurons is regulated by membrane depolarization and suggest a novel Ca2+-responsive promoter element. Through this mechanism, IL-6 may function as a neuromodulator induced by neuronal activity. 
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