title: Exogenous nitric oxide-induced release of calcium from intracellular IP3 receptor-sensitive stores via S-nitrosylation in respiratory burst-dependent neutrophils.
abstract: PMA-induced respiratory burst neutrophils were exposed to exogenous nitric oxide (NO) donor sodium nitroprusside (SNP) to study the effect of NO on calcium signaling. A sharp rise of cytosolic calcium concentration ([Ca(2+)](c)) was triggered by 1mM SNP with and without external calcium. We found that GF 109203X, a specific inhibitor of protein kinase C, DPI, a putative inhibitor of the respiratory burst-generating NADPH oxidase, and 2-DG, a non-metabolizable analog of glucose, completely inhibited the SNP-induced rise of [Ca(2+)](c) in PMA-activated respiratory burst neutrophils. Meanwhile, 2-APB and TMB-8, two potent IP(3) receptor inhibitors, prevented calcium increase respectively. Furthermore, N-ethylmaleimide (NEM), a specific cysteine alkylating agent, evidently abolished the [Ca(2+)](c) elevation. In contrast, the sGC inhibitor NS2028 had little effect on the rise of [Ca(2+)](c). Taken together, these results indicated that exogenous NO induced the release of calcium from intracellular IP(3) receptor-sensitive stores of neutrophils via S-nitrosylation in a respiratory burst-dependent manner.
authors.affiliation: The Key Laboratory of Weak-Light Nonlinear Photonics, Ministry of Education, Institute of Physics and TEDA Applied Physics School, Nankai University, Tianjin 300457, China.
authors.forename: Leiting
authors.initials: L
authors.lastname: Pan
authors.forename: Xinzheng
authors.initials: X
authors.lastname: Zhang
authors.forename: Kun
authors.initials: K
authors.lastname: Song
authors.forename: Xian
authors.initials: X
authors.lastname: Wu
authors.forename: Jingjun
authors.initials: J
authors.lastname: Xu
mesh_terms: D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D006801:Humans; D007211:Indoles / Q000494:pharmacology; D053496:Inositol 1,4,5-Trisphosphate Receptors / Q000378:metabolism*; D008301:Maleimides / Q000494:pharmacology; D009504:Neutrophils / Q000187:drug effects / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism* / Q000494:pharmacology; D020030:Nitric Oxide Donors / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D047428:Protein Kinase Inhibitors / Q000494:pharmacology; D016897:Respiratory Burst; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology
chemical_list: D007211:Indoles; D053496:Inositol 1,4,5-Trisphosphate Receptors; D008301:Maleimides; D020030:Nitric Oxide Donors; D047428:Protein Kinase Inhibitors; D009599:Nitroprusside; D009569:Nitric Oxide; D011493:Protein Kinase C; C070515:bisindolylmaleimide I; D013755:Tetradecanoylphorbol Acetate; D002118:Calcium