Oxidative stress increases A1 adenosine receptor expression by activating nuclear factor kappa B.

摘要: The A1 adenosine receptor (A1AR) contributes to the cytoprotective action of under conditions known generate reactive oxygen species (ROS). Pharmacological manipulation A1AR expression has been shown modulate this role. In study, we provide evidence that ROS generated could increase and thereby offset detrimental effects ROS. Incubation DDT1MF-2 smooth muscle cells with ROS-generating chemotherapeutic agents, such as cisplatin (2.5 μm) or H2O2 (10 μm), elicited an in within 24 hr. induction by was reduced scavenger catalase but not superoxide dismutase. Inhibition nuclear factor κB (NFκB) pyrrolidine dithiocarbamate (200 dexamethasone (100 nm), genistein (1 abrogated cisplatin-mediated A1AR. Cisplatin promoted rapid translocation NFκB (but AP-1) nucleus, detected electrophoretic mobility shift assays Western blotting. A putative sequence promoter effectively competed labeled probe for binding preparations derived from cells. Transient transfection coupled firefly luciferase reporter gene led cisplatin-inducible dithiocarbamate-sensitive activity, suggesting presence functional site(s) sequence. Treatment (R)-phenylisopropyladenosine agonist A1AR, lipid peroxidation, which reversed after blockade These data suggest can activating regulatory on enhance role adenosine.