ArticleNeuroscience bulletin2009
Initial bradykinin triggers calcium-induced calcium release in C6 glioma cells and its significance.
Article in Neuroscience bulletin, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Bradykinin-mediated CaJournal of cellular and molecular medicine · 2018Article
- The Role of HOTAIR/miR-148b-3p/USF1 on Regulating the Permeability of BTB.Frontiers in molecular neuroscience · 2017Article
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Authors and funding
2 authors.
Funding
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Abstract
objectiveTo investigate the underlying mechanism for the selective modulation of the permeability of blood-tumor barrier (BTB) by small dose of bradykinin (BK).
methodsC6 glioma cells were treated with BK, and changes of intracellular nitric oxide (NO) and intracellular calcium level were measured with fluorescent spectrophotometer.
resultsThe initial application of BK easily triggered extracellular calcium influx, which resulted in intracellular calcium store release in C6 glioma cells. The above mechanism was also named ryanodine mediated calcium induced calcium release (CICR). We also detected a long-lasting intracellular NO elevation in C6 glioma cells upon BK treatment. Further study showed that ryanodine mediated CICR contributed greatly to the secondary NO elevation induced by BK treatment.
conclusionThese results suggested that BK triggered CICR in C6 glioma cells and the associated NO generation might be the underlying mechanism for the selective modulation of BTB permeability by BK.
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