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Category:Computer-aided design software for WindowsEvidence is increasingly accumulating that PDE11A is the major determinant of β2 adrenoceptor-mediated cAMP signalling in airway smooth muscle.
β2 adrenoceptor (β2-AR) agonists play a central role in asthma control, but their use is limited by their adverse effects (AEs) such as bronchoconstriction, especially during exercise. Thus, it is important to understand the mechanisms that underlie β2-AR signalling in the airways. In this study, we investigated the role of PDE11A in β2-AR signalling in the airways. The human β2-AR phosphodiesterase-11A (hPDE11A) was overexpressed in HEK-293 cells by transient transfection and the cAMP signal transduction pathway was investigated by evaluating the concentration-response relationship and by evaluating the effects of PDE11A inhibition with the phosphodiesterase-11A (PDE11A) inhibitor forskolin (FSK) or vinpocetine. Moreover, the expression of the PDE11A protein and mRNA, and the effects of the PDE11A inhibitor on β2-AR signalling were analysed in β2-AR deficient mice, and PDE11A was overexpressed in airway smooth muscle (ASM) cells from C57BL/6 mice. The PDE11A-mediated cAMP signals in β2-AR overexpression was inhibited by the PDE11A inhibitors, FSK and vinpocetine. β2-AR deficient mice had increased cAMP-dependent protein kinase (PKA) phosphorylation compared with wild-type mice. ASM cells from C57BL/6 mice also showed a decreased PDE11A protein expression and activity with FSK treatment. FSK treatment decreased protein kinase A (PKA) phosphorylation, myosin light chain phosphorylation and cell shortening in ASM cells, but the effects were not significant on β2-AR-coupled cAMP production. However, cAMP signalling was decreased in C57BL/6 airway smooth muscle cells, but not in HEK-293 cells transfected with hPDE11A, by the PDE11A inhibitor, vinpocetine. P