Low dose of bradykinin selectively increases intracellular calcium in glioma cells

Wang, Yibao; Peng, Cheng; Liu, Yunhui

doi:10.1016/j.jns.2007.02.031

Cited by 29 publications

(37 citation statements)

References 15 publications

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“…2C) and 1×10 -5 mol/L BK in astrocytes could not trigger such calcium response [7] . Therefore we proposed that this wider calcium peak might contribute to the secondary NO release after initial BK treatment.…”

Section: Discussionmentioning

confidence: 92%

“…4A), but 1×10 -5 mol/L BK, which could trigger intracellular calcium elevation in astrocytes [7] , could not trigger NO release.…”

Section: Discussionmentioning

confidence: 92%

“…Importantly, the initial BK triggered a long-lasting calcium elevation in C6 glioma cell compared to astrocytes. However, BMECs could not express B 2 receptor and was not the direct target of BK [7] .…”

Section: Discussionmentioning

confidence: 96%

“…Since extracellular calcium influx is the prerequisite for the intracellular calcium peak formation, it seems that BK causes extracellular calcium influx, which triggers ryanodine-sensitive mediated calcium store release. This type of intracellular calcium elevation is called CICR [6,7] , a mechanism for calcium release from internal stores. C6 glioma cells and astrocytes, like many other cell types, express Ca 2+ -sensitive RyRs in their smooth ER membrane.…”

Section: Discussionmentioning

confidence: 99%

“…Previously, it is demonstrated that small doses of BK could selectively activate intracellular calcium release in C6 glioma cells and BK could easily elicit peak-after plateau, shoulder formation and sometimes a second Ca 2+ peak in C6 glioma cells when compared to astrocytes [7] . In this study we found that the above observation resulted from a delayed calcium transient following calcium peak and that RyRs medicated calcium store release contributed to this delayed calcium transient, which contributed to long-lasting intracellular nitric oxide (NO) elevation in C6 glioma cells after BK treatment.…”

Section: Calcium-induced Calcium Release (Cicr) Is a Mechanismmentioning

confidence: 99%

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

Wang

Liu

2009

Neurosci. Bull.

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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 longlasting 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.

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Section: Discussionmentioning

confidence: 92%

“…4A), but 1×10 -5 mol/L BK, which could trigger intracellular calcium elevation in astrocytes [7] , could not trigger NO release.…”

Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 96%

Section: Discussionmentioning

confidence: 99%

Section: Calcium-induced Calcium Release (Cicr) Is a Mechanismmentioning

confidence: 99%

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

Wang

Liu

2009

Neurosci. Bull.

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Inverse correlation of intracellular calcium and cyclic AMP levels in renal cell carcinoma

Sharma

Singh

Prasad

2012

Cell Biochemistry & Function

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Renal cell carcinoma (RCC) is the most common renal tumour in adults. Altered levels of secondary messengers, that is, intracellular calcium and cyclic AMP (cAMP), have been implicated in the pathogenesis of various malignancies. In the present study, we measured levels of intracellular calcium and cAMP in RCC. The intracellular calcium level was significantly reduced, whereas the cAMP level was significantly augmented in RCC as compared with adjacent grossly normal renal parenchyma.

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Glioblastoma‐mesenchymal stem cell communication modulates expression patterns of kinin receptors: Possible involvement of bradykinin in information flow

et al. 2015

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The most aggressive subtype of brain tumors is glioma WHO grade IV, the glioblastoma (GBM). The present work aims to elucidate the role of kinin receptors in interactions between GBM cells and mesenchymal stem cells (MSC). The GBM cell line U87-MG was stably transfected to express dsRed protein, single cell cloned, expanded, and cultured with MSC, both in the direct co-cultures (DC) and indirect co-cultures (IC) at equal cell number ratio for 72 h. Up-and down-regulation of matrix metalloproteases (MMP)29 expression in U87-MG and MSC cells, respectively, in direct coculture points to possible MSC participation in tumor invasion. MMP9 expression is in line with significantly increased expression of kinin B1 (B1R) and B2 receptor (B2R) in U87-MG cells and their decreased levels in MSC, as confirmed by quantitative assessment using flow cytometric analysis. Similarly, in indirect cultures (IC), lacking the contact between GBM and MSC cells, an increase of B1 and B2 receptor expression was again noted in U87-MG cells, and no significant changes in kinin receptors in MSC was observed. Functionality of kinin-B1 and B2 receptors was evidenced by stimulation of intracellular calcium fluxes by their respective agonists, des-Arg9-bradykinin (DBK) and bradykinin (BK). Moreover, BK showed a feedback control on kinin receptor expression in mono-cultures, direct and indirect co-cultures. The treatment with BK resulted in down-regulation of B1 and B2 receptors in MSC, with simultaneous upregulation of these receptors in U87-MG cells, suggesting that functions of BK in information flow between these cells is important for tumor progression and invasion. V C International Society for Advancement of CytometryKey terms Bradykinin; kinin-B1 receptor; kinin-B2 receptor; glioblastoma; bone-marrow mesenchymal stem cells; direct and indirect cell co-culture GLIOMAS, although classified as a rare neoplastic disease, are still the most frequent brain tumors and their most malignant form (WHO stage IV astrocytoma). Glioblastoma (GBM) has an average postoperative survival of only 14.6 or 12.1 months when treated with radio-and chemo-therapy (temozolomide) or with radiotherapy alone, respectively (1). The major characteristic of these tumors is the high infiltration rate of single cells, the so called "guerrilla" cells into the brain parenchyma, even several cm away from the bulk tumor mass. These cells are hard to target by conventional therapies. In view of that, the development of novel therapeutic strategies for successful GBM treatment targeting tumor invasiveness has turned into an aim of priority.

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Low dose of bradykinin selectively increases intracellular calcium in glioma cells

Cited by 29 publications

References 15 publications

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

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

Inverse correlation of intracellular calcium and cyclic AMP levels in renal cell carcinoma

Glioblastoma‐mesenchymal stem cell communication modulates expression patterns of kinin receptors: Possible involvement of bradykinin in information flow

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