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. 2009 Feb 4;25(1):21. doi: 10.1007/s12264-009-1125-7

Initial bradykinin triggers calcium-induced calcium release in C6 glioma cells and its significance

缓激肽触发 C6 胶质瘤细胞内 Ca2+ 内流诱发的 Ca2+ 释放

Yi-Bao Wang 1,, Yun-Hui Liu 2
PMCID: PMC5552498  PMID: 19190685

Abstract

Objective

To investigate the underlying mechanism for the selective modulation of the permeability of blood-tumor barrier (BTB) by small dose of bradykinin (BK).

Methods

C6 glioma cells were treated with BK, and changes of intracellular nitric oxide (NO) and intracellular calcium level were measured with fluorescent spectrophotometer.

Results

The 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.

Conclusion

These 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.

Keywords: bradykinin, blood brain barrier, glioma

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