Linked Life Data

9326272

Source:http://linkedlifedata.com/resource/pubmed/id/9326272

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pubmed-article:9326272pubmed:abstractTextWe have examined the effect of elevating cyclic AMP levels on cytokine-mediated enhancement of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) gene expression by astrocytes. Treatment of astrocytes with the cyclic AMP mimetic dibutyryl-cyclic AMP, or the agonists norepinephrine, forskolin, prostaglandin E2, and cholera toxin alone had no effect on ICAM-1 or VCAM-1 mRNA gene expression. However, elevating cyclic AMP levels within the cells by these agents suppressed interleukin-1beta- and tumor necrosis factor-alpha-induced adhesion molecule expression at both the mRNA and protein levels. The phosphodiesterase type IV inhibitor, rolipram, was able to potentiate the inhibitory effect of forskolin on ICAM-1 and VCAM-1 gene expression. Inhibition of tumor necrosis factor-alpha-induced VCAM-1 mRNA levels by forskolin was partially due to enhanced degradation of VCAM-1 message, whereas the decay rates of tumor necrosis factor-alpha-induced ICAM-1 message and interleukin-1beta-induced ICAM-1/VCAM-1 message were not affected by forskolin treatment. These results demonstrate that the pathways used by interleukin-1beta and tumor necrosis factor-alpha to induce adhesion molecule expression are antagonized by cyclic AMP-dependent protein kinase-mediated signaling pathways.lld:pubmed
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pubmed-article:9326272pubmed:dateRevised2007-11-14lld:pubmed
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pubmed-article:9326272pubmed:articleTitleElevation of cyclic AMP levels in astrocytes antagonizes cytokine-induced adhesion molecule expression.lld:pubmed
pubmed-article:9326272pubmed:affiliationDepartment of Cell Biology, University of Alabama at Birmingham, 35294-0005, U.S.A.lld:pubmed
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pubmed-article:9326272pubmed:publicationTypeResearch Support, U.S. Gov't, P.H.S.lld:pubmed
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