Exogenous nitric oxide-induced release of calcium from intracellular IP3 receptor-sensitive stores via S-nitrosylation in respiratory burst-dependent neutrophils |
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Authors: | Leiting Pan |
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Institution: | The Key Laboratory of Weak-Light Nonlinear Photonics, Ministry of Education, Institute of Physics and TEDA Applied Physics School, Nankai University, Tianjin 300457, China |
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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 (Ca2+]c) was triggered by 1 mM 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 Ca2+]c in PMA-activated respiratory burst neutrophils. Meanwhile, 2-APB and TMB-8, two potent IP3 receptor inhibitors, prevented calcium increase respectively. Furthermore, N-ethylmaleimide (NEM), a specific cysteine alkylating agent, evidently abolished the Ca2+]c elevation. In contrast, the sGC inhibitor NS2028 had little effect on the rise of Ca2+]c. Taken together, these results indicated that exogenous NO induced the release of calcium from intracellular IP3 receptor-sensitive stores of neutrophils via S-nitrosylation in a respiratory burst-dependent manner. |
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Keywords: | Nitric oxide SNP S-Nitrosylation PMA Calcium IP3 receptor-sensitive stores Respiratory burst-dependent Neutrophils |
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