Mechanisms of bradykinin-mediated Ca2+ signalling in canine cultured corneal epithelial cells

Huang, Song‐Chei; Chien, Chin-Sung; Hsiao, Li-Der; Wang, Chuan-Chwan; Chiu, Chi‐Tso; Liang, Kao-Yi; Yang, Chih-Hui

doi:10.1016/s0898-6568(01)00170-x

Cited by 7 publications

(11 citation statements)

References 42 publications

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“…The authors concluded that in these cells bradykinin induces Ca 2+ influx independent of store depletion, and thus it appeared that only non-CCE could have accounted for the bradykinin-induced Ca 2+ influx [16]. In the present study, we carefully designed the protocols and demonstrated that bradykinin can induce Ca 2+ influx via both CCE and non-CCE.…”

Section: Discussionmentioning

confidence: 67%

“…One previous study by Huang et al [16] has investigated the bradykinin-induced Ca 2+ influx in canine corneal endothelial cells. The authors concluded that in these cells bradykinin induces Ca 2+ influx independent of store depletion, and thus it appeared that only non-CCE could have accounted for the bradykinin-induced Ca 2+ influx [16].…”

Section: Discussionmentioning

confidence: 99%

“…We believe that the discrepancy in results is at least partly due to inappropriate control in their report. Huang et al [16] compared the bradykinin-induced Ca 2+ influx between the cells with or without store depletion (using thapsigargin pretreatment for store depletion) and concluded that bradykinin-induced Ca 2+ influx was not affected by the store depletion (with thapsigargin) [16]. However, in their control group, in which Ca 2+ stores were not supposed to be depleted, agonist (bradykinin) was present, which would inevitably lead to store depletion.…”

Section: Discussionmentioning

confidence: 99%

“…Because bradykinin may stimulate the production of many of these second messengers, it is expected that bradykinin should be able to induce non-CCE. However, up to the present there are only a few studies investigating bradykinin-induced non-CCE in endothelial cells [16, 17]. The signal transduction pathways and ion channels that mediate bradykinin-induced non-CCE in endothelial cells are poorly defined.…”

Section: Introductionmentioning

confidence: 99%

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Mechanism of Non-Capacitative Ca<sup>2+</sup> Influx in Response to Bradykinin in Vascular Endothelial Cells

Leung¹,

Cheng²,

Liu³

et al. 2006

J Vasc Res

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Bradykinin is a potent vasoactive nonapeptide. It elicits a rise in cytosolic Ca²⁺ (Ca²⁺)_i in endothelial cells, resulting in Ca²⁺-dependent synthesis and release of endothelial vasodilators. In the present study, we investigated the mechanism of bradykinin-induced Ca²⁺ influx in primary cultured rat aortic endothelial cells and in a mouse heart microvessel endothelial cell line (H5V). Bradykinin-induced Ca²⁺ influx was resolved into capacitative Ca²⁺ entry (CCE) and non-CCE. The non-CCE component was inhibited by a B2 receptor antagonist (HOE140; 1 µM) and a phospholipase C (PLC) inhibitor (U73122; 10 µM). The action of bradykinin could be mimicked by 1-oleoyl-2-acetyl-glycerol, an analogue of diacylglycerol (DAG), and by RHC80267, a DAG-lipase inhibitor. Immunoblots showed that TRPC6 was one of the main TRPC channels expressed in endothelial cells. Transfection of H5V cells with two siRNA constructs against TRPC6 both markedly reduced the TRPC6 protein level and, at the same time, decreased the percentage of cells displaying bradykinin-induced non-CCE. siRNA transfection also reduced the magnitude of non-CCE among the cells responding to bradykinin. Taken together, our data suggest that bradykinin-induced non-CCE is mediated via the B2-PLC pathway, and that DAG may be involved in this process. Further, TRPC6 is one of the important channels participating in bradykinin-induced non-CCE in endothelial cells.

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Section: Discussionmentioning

confidence: 67%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Mechanism of Non-Capacitative Ca<sup>2+</sup> Influx in Response to Bradykinin in Vascular Endothelial Cells

Leung¹,

Cheng²,

Liu³

et al. 2006

J Vasc Res

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“…In particular, BK can stimulate both capacitative [34] and non-capacitative Ca 2+ entry in endothelial cells [21,36-38]. To define the action of vasoinhibins in BK-induced extracellular Ca 2+ entry, we quantified the amount of Ca 2+ released from the endoplasmic reticulum and measured the magnitude of the Ca 2+ entry in response to the addition of 2 mM Ca 2+ to the bath solution.…”

Section: Resultsmentioning

confidence: 99%

Vasoinhibins Prevent Bradykinin-Stimulated Endothelial Cell Proliferation by Inactivating eNOS via Reduction of both Intracellular Ca2+ Levels and eNOS Phosphorylation at Ser1179

et al. 2011

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Vasoinhibins, a family of antiangiogenic peptides derived from prolactin proteolysis, inhibit the vascular effects of several proangiogenic factors, including bradykinin (BK). Here, we report that vasoinhibins block the BK-induced proliferation of bovine umbilical vein endothelial cells. This effect is mediated by the inactivation of endothelial nitric oxide synthase (eNOS), as the NO donor DETA-NONOate reverted vasoinhibin action. It is an experimentally proven fact that the elevation of intracellular Ca2+ levels ([Ca2+]i) upon BK stimulation activates eNOS, and vasoinhibins blocked the BK-mediated activation of phospholipase C and the formation of inositol 1,4,5-triphosphate leading to a reduced release of Ca2+ from intracellular stores. The [Ca2+]i rise evoked by BK also involves the influx of extracellular Ca2+ via canonical transient receptor potential (TRPC) channels. Vasoinhibins likely interfere with TRPC-mediated Ca2+ entry since La3+, which is an enhancer of TRPC4 and TRPC5 channel activity, prevented vasoinhibins from blocking the stimulation by BK of endothelial cell NO production and proliferation, and vasoinhibins reduced the BK-induced increase of TRPC5 mRNA expression. Finally, vasoinhibins prevented the BK-induced phosphorylation of eNOS at Ser1179, a post-translational modification that facilitates Ca2+-calmodulin activation of eNOS. Together, our data show that vasoinhibins, by lowering NO production through the inhibition of both [Ca2+]i mobilization and eNOS phosphorylation, prevent the BK-induced stimulation of endothelial cell proliferation. Thus, vasoinhibins help to regulate BK effects on angiogenesis and vascular homeostasis.

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Bradykinin-stimulated p42/p44 MAPK activation associated with cell proliferation in corneal keratocytes

Cheng

Huang

Hsiao

et al. 2004

Cellular Signalling

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Mechanisms of bradykinin-mediated Ca2+ signalling in canine cultured corneal epithelial cells

Cited by 7 publications

References 42 publications

Mechanism of Non-Capacitative Ca<sup>2+</sup> Influx in Response to Bradykinin in Vascular Endothelial Cells

Mechanism of Non-Capacitative Ca<sup>2+</sup> Influx in Response to Bradykinin in Vascular Endothelial Cells

Vasoinhibins Prevent Bradykinin-Stimulated Endothelial Cell Proliferation by Inactivating eNOS via Reduction of both Intracellular Ca2+ Levels and eNOS Phosphorylation at Ser1179

Bradykinin-stimulated p42/p44 MAPK activation associated with cell proliferation in corneal keratocytes

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