Pharmacological and Functional Characterization of Bradykinin Receptors in Rat Cultured Vascular Smooth Muscle Cells

Yang, Che‐Hua; Tsai, Yih Jeng; Pan, Shiow Lin; Wu, Wen Bin; Wang, Chuan Chwan; Lee, Ying Shiung; Lin, Chih Chung; Huang, Song‐Chei; Chiu, Chi Tso

doi:10.1016/s0898-6568(99)00056-x

Cited by 22 publications

(27 citation statements)

References 34 publications

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“…The bradykinin-induced response was inhibited by nifedipine and verapamil (30). In the present study, the release of ATP evoked by the peptide was attenuated by nifedipine and verapamil, voltagegated Ca…”

Section: +supporting

confidence: 58%

“…Then the cells were kept for 25 min in the solution (37°C) with and without test antagonists. After the cells had been exposed to the agonist, the dish medium was replaced with 1% PCA solution (pH 1.11) or the cell lysis buffer containing 1% Triton-X at each time point (10,20,30, and 60 s). The experiment with the PCA solution was undertaken as follows.…”

Section: Cytosolic Accumulation Of Atpmentioning

confidence: 99%

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Endoplasmic Reticulum Is a Key Organella in Bradykinin-Triggered ATP Release From Cultured Smooth Muscle Cells

et al. 2007

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Abstract. ATP has broad functions as an autocrine / paracrine molecule. The mode of ATP release and its intracellular source, however, are little understood. Here we show that bradykinin via B 2 -receptor stimulation induces the extracellular release of ATP via the inositol 1,4,5-trisphosphate [Ins(1,4,5)P 3 ]-signaling pathway in cultured taenia coli smooth muscle cells. It was found that bradykinin also increased the production of Ins(1,4,5)P 3 and 2-APB-inhibitable [CaThe evoked release of ATP was suppressed by the Ca 2+ -channel blockers, nifedipine, and verapamil. Moreover, the extracellular release of ATP was elicited by photoliberation of Ins(1,4,5)P 3 . Bradykinin caused a quick and transient accumulation of intracellular ATP from cells treated with 1% perchloric acid solution (PCA), but not with the cell lysis buffer. Peak accumulation was prevented by 2-APB and thapsigargin, but not by nifedipine or verapamil, inhibitors of extracellular release of ATP. These findings suggest that bradykinin elicits the extracellular release of ATP that is mediated by the Ins(1,4,5)P 3 -induced Ca 2+ signaling and, finally, leads to a Ca 2+-dependent export of ATP from the cells. Furthermore, the bradykinininduced transient accumulation of ATP in the cells treated with PCA may imply a possible release of ATP from the endoplasmic reticulum.

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Section: +supporting

confidence: 58%

Section: Cytosolic Accumulation Of Atpmentioning

confidence: 99%

Endoplasmic Reticulum Is a Key Organella in Bradykinin-Triggered ATP Release From Cultured Smooth Muscle Cells

et al. 2007

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“…VSMCs were stimulated with bradykinin (10 Ϫ6 mol/l), acutely (10 -30 min) or chronically (1-24 h). In some experiments, cells were preexposed for 30 min to Hoe-140 [bradykinin-2 (B 2) receptor antagonist; 10 Ϫ5 mol/l], chelerythrine (PKC inhibitor; 10 Ϫ5 mol/l), U-73122 (PLC inhibitor; 10 Ϫ5 mol/l) or 2-aminoethoxydiphenyl borate (2-APB; TRPM7 inhibitor; 10 Ϫ5 mol/l, 2 h pretreatment) (18,50,52).…”

Section: Methodsmentioning

confidence: 99%

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Yogi¹,

Callera²,

Tostes³

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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Yogi A, Callera GE, Tostes R, Touyz RM. Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells. Am J Physiol Regul Integr Comp Physiol 296: R201-R207, 2009. First published September 17, 2008 doi:10.1152/ajpregu.90602.2008.-Transient receptor potential melastatin-7 (TRPM7) channels have recently been identified to be regulated by vasoactive agents acting through G protein-coupled receptors in vascular smooth muscle cells (VSMC). However, downstream targets and functional responses remain unclear. We investigated the subcellular localization of TRPM7 in VSMCs and questioned the role of TRPM7 in proinflammatory signaling by bradykinin. VSMCs from Wistar-Kyoto rats were studied. Cell fractionation by sucrose gradient and differential centrifugation demonstrated that in bradykinin-stimulated cells, TRPM7 localized in fractions corresponding to caveolae. Immunofluorescence confocal microscopy revealed that TRPM7 distributes along the cell membrane, that it has a reticular-type intracellular distribution, and that it colocalizes with flotillin-2, a marker of lipid rafts. Bradykinin increased expression of calpain, a TRPM7 target, and stimulated its cytosol/membrane translocation, an effect blocked by 2-APB (TRPM7 inhibitor) and U-73122 (phospholipase C inhibitor), but not by chelerythrine (PKC inhibitor). Expression of proinflammatory mediators VCAM-1 and cyclooxygenase-2 (COX-2) was time-dependently increased by bradykinin. This effect was blocked by Hoe-140 (B 2 receptor blocker) and 2-APB. Our data demonstrate that in bradykinin-stimulated VSMCs: 1) TRPM7 is upregulated, 2) TRPM7 associates with cholesterol-rich microdomains, and 3) calpain and proinflammatory mediators VCAM-1 and COX2 are regulated, in part, via TRPM7-and phospholipase C-dependent pathways through B 2 receptors. These findings identify a novel signaling pathway for bradykinin, which involves TRPM7. Such phenomena may play a role in bradykinin/B 2 receptor-mediated inflammatory responses in vascular cells.

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“…Activation of both receptors promotes intracellular calcium mobilization by inositol 1,4,5-triphosphate, production by phospholipase C-beta activity, and evoke release of nitric oxide and prostaglandins (Marceau and Regoli, 2004;Thornton et al, 2010). Both receptor subtypes are expressed by many cell types, including neurons (Couture et al, 2001), glial cells (Gimpl et al, 1992;Stephens et al, 1993;Noda et al, 2003), endothelial cells (Miyamoto et al, 1999) and vascular smooth muscle cells (Yang et al, 1999). In the human brain, components of KKS were found specifically in the thalamus, hypothalamus, cerebral cortex and spinal cord (Raidoo and Bhoola, 1997).…”

Section: The Kallikrein-kinin Systemmentioning

confidence: 99%

Kinins and microglial responses in bipolar disorder: a neuroinflammation hypothesis

Naaldijk¹,

Bittencourt²,

Sack

et al. 2016

Biological Chemistry

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Bipolar disorder (BD) is a severe psychiatric disorder that affects up to 15% of the worldwide population. Characterized by switches in mood between mania and depression, its etiology is still unknown and efforts have been made to elucidate the mechanisms involved in first episode, development and progression of the disorder. Microglia activation, abnormal activity of GSK-3β and reduction in neurotrophic factor expression related to neuroinflammatory processes have been indicated to be part of the disorder's pathophysiology. Lithium, the main mood stabilizer used for the treatment and prevention of relapses, acts as an anti-inflammatory agent. Based on that, here we suggest a neuroinflammatory pathway for would be BD progression, in which microglia activation states modulated via constitutive induction of kinin-B1 receptor and reduction of kinin-B2 receptor expression and activity.

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Pharmacological and Functional Characterization of Bradykinin Receptors in Rat Cultured Vascular Smooth Muscle Cells

Cited by 22 publications

References 34 publications

Endoplasmic Reticulum Is a Key Organella in Bradykinin-Triggered ATP Release From Cultured Smooth Muscle Cells

Endoplasmic Reticulum Is a Key Organella in Bradykinin-Triggered ATP Release From Cultured Smooth Muscle Cells

Bradykinin regulates calpain and proinflammatory signaling through TRPM7-sensitive pathways in vascular smooth muscle cells

Kinins and microglial responses in bipolar disorder: a neuroinflammation hypothesis

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