Signaling molecules play a critical role in the pathophysiology of airway diseases. Recent evidence shows that cyclic ADP-ribose (cADPr), an endogenous activator of the ryanodine receptor channel in mammalian cells, modulates agonist-induced calcium responses in airway smooth muscle (ASM) cells. In addition, cADPr-mediated calcium release appears to play an important role in the 'non-specific' increased ASM responsiveness to contractile agonists in cytokine-treated cells, a characteristic finding of asthma. Furthermore, other signaling molecules such as Rho/Rho kinase and phosphodiesterase also contribute to bronchial hyperresponsiveness. Thus, a better understanding of these signaling molecules that alter calcium signaling and contractility of ASM might provide new insight into novel therapeutic targets for the control of bronchial hyperresponsiveness.
Bibliographical noteFunding Information:
Supported by NIH grants 2R01-HL55301 (RAP) and 1P50-HL67663 (RAP), 2RO1-HL57498 (MSK), DA11806 (TFW) and by an American Lung Association grant RG-062-N (YA). Yassine Amrani is a Parker B Francis Fellow in Pulmonary Research.
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