ArticleThe Biochemical journal1997
Chemoattractant-induced respiratory burst: increases in cytosolic Ca2+ concentrations are essential and synergize with a kinetically distinct second signal.
Article in The Biochemical journal, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 75 citations in OpenAlex.
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- Calcium Release from Endoplasmic Reticulum Involves Calmodulin-Mediated NADPH Oxidase-Derived Reactive Oxygen Species Production in Endothelial Cells.International journal of molecular sciences · 2019Article
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- TRPC3 Channels in Cardiac Fibrosis.Frontiers in cardiovascular medicine · 2017Review
- Inhibition of neutrophil superoxide generation by shikonin is associated with suppression of cellular Ca(2+) fluxes.Journal of clinical biochemistry and nutrition · 2016Article
- The role of STIM and ORAI proteins in phagocytic immune cells.American journal of physiology. Cell physiology · 2016Review
- The role of selenium in inflammation and immunity: from molecular mechanisms to therapeutic opportunities.Antioxidants & redox signaling · 2012Review
- Characterization of superoxide overproduction by the D-Loop(Nox4)-Nox2 cytochrome b(558) in phagocytes-Differential sensitivity to calcium and phosphorylation events.Biochimica et biophysica acta · 2011Article
- Regulation of phagocyte NADPH oxidase by hydrogen peroxide through a Ca(2+)/c-Abl signaling pathway.Free radical biology & medicine · 2010Article
- Inhibitors of TRP channels reveal stimulus-dependent differential activation of Ca2+ influx pathways in human neutrophil granulocytes.Naunyn-Schmiedeberg's archives of pharmacology · 2009Article
- Regulation of superoxide production in neutrophils: role of calcium influx.Journal of leukocyte biology · 2008Review
- The two neutrophil members of the formylpeptide receptor family activate the NADPH-oxidase through signals that differ in sensitivity to a gelsolin derived phosphoinositide-binding peptide.BMC cell biology · 2004Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The role of the cytosolic free Ca2+ concentration ([Ca2+]c) and its relationship to other second messengers in the signalling between chemoattractant [e.g. N-formyl-l-methionyl-l-leucyl-l-phenylalanine (fMLP)] receptors and the NADPH oxidase is still poorly understood. In this study, we have used thapsigargin, an inhibitor of the Ca2+-ATPase of intracellular stores, as a tool to selectively manipulate Ca2+ release from intracellular stores and Ca2+ influx across the plasma membrane. We thereby temporarily separated the Ca2+ signal from other signals generated by fMLP and analysed the consequences on the respiratory burst. Under all conditions investigated, the extent of fMLP-induced respiratory burst activation was critically determined by [Ca2+]c elevation. fMLP was unable to activate the respiratory burst without [Ca2+]c elevation. Thapsigargin-induced Ca2+ influx activated the respiratory burst in the absence of fMLP, but only to approx. 20% of the values observed in the presence of fMLP. The second signal generated by fMLP did not activate the respiratory burst by itself, but acted in synergy with [Ca2+]c elevation. The second signal was long lasting (>15 min) provided that there was no rise in [Ca2+]c and that the receptor was continuously occupied. The second signal was inactivated by high [Ca2+]c elevation. Our results demonstrate that [Ca2+]c elevations are an essential step in the signalling between the fMLP receptor and NADPH oxidase. They also provide novel information about the properties of the second Ca2+-independent signal that activates the respiratory burst in synergy with [Ca2+]c.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.