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• W1991750302 abstract "Abstract: During cerebral ischemia, the expression of interleukin-6 (IL-6), which has neuroprotective properties, increases. To understand the underlying mechanism, the regulation of IL-6 expression by neurotransmitters that accumulate during cerebral ischemia was investigated. Adenosine stimulated IL-6 secretion in primary astrocytes four- to 10-fold. The effect was concentration dependent, the EC50 being ∼8 µM. Although the nonselective analogue 2-chloroadenosine (2CA) increased IL-6 secretion to a similar extent, the A1-selective agonist N6-cyclopentyladenosine or the A2a agonist CGS-21680 had only a marginal effect on IL-6 secretion. IL-6 secretion stimulated by 2CA (10 µM) was inhibited by the nonselective adenosine antagonist 8-(p-sulfophenyl)theophylline, whereas the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine or the A2a-selective antagonist 8-(3-chlorostyryl)caffeine had no effect, to a concentration of 0.1 µM. Transcription of the IL-6 gene was investigated by transfecting primary astrocytes with a reporter fusion gene containing the human IL-6 promoter (−179/+12). 2CA stimulated IL-6 gene transcription 2.5-fold. Mutations of the binding site for NF-κB or NF-IL6 abrogated the response to 2CA. Thus, an increase of extracellular adenosine during focal cerebral ischemia may stimulate IL-6 expression via A2b receptors. The induction of IL-6 expression appears to involve a transcriptional effect that depends on NF-κB and NF-IL6." @default.
• W1991750302 created "2016-06-24" @default.
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• W1991750302 date "2002-11-18" @default.
• W1991750302 modified "2023-09-23" @default.
• W1991750302 title "Stimulation of Interleukin-6 Secretion and Gene Transcription in Primary Astrocytes by Adenosine" @default.
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• W1991750302 doi "https://doi.org/10.1046/j.1471-4159.1997.69031145.x" @default.
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