Effect of I?2-adrenoceptor agonists and other cAMP-elevating agents on inflammatory gene expression in human ASM cells: a role for protein kinase A
- American Physiological Society
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- Journal Article
- Newton, Robert et al. 2008, 'Effect of I?2-adrenoceptor agonists and other cAMP-elevating agents on inflammatory gene expression in human ASM cells: a role for protein kinase A', American Journal of Physiology: Lung Cellular and Molecular Physiology, vol. 295, no. 3, pp. L505-L514.
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In diseases such as asthma, airway smooth muscle (ASM) cells play a synthetic role by secreting inflammatory mediators such as granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-6, or IL-8 and by expressing surface adhesion molecules, including ICAM-1. In the present study, PGE2, forskolin, and short-acting (salbutamol) and long-acting (salmeterol and formoterol) I?2-adrenoceptor agonists reduced the expression of ICAM-1 and the release of GM-CSF evoked by IL-1I? in ASM cells. IL-1I?-induced IL-8 release was also repressed by PGE2 and forskolin, whereas the I?2-adrenoceptor agonists were ineffective. In each case, repression of these inflammatory indexes was prevented by adenoviral overexpression of PKIa, a highly selective PKA inhibitor. These data indicate a PKA-dependent mechanism of repression and suggest that agents that elevate intracellular cAMP, and thereby activate PKA, may have a widespread anti-inflammatory effect in ASM cells.
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