Molecular cloning of prostaglandin EP3 receptors from canine sensory ganglia and their facilitatory action on bradykinin‐induced mobilization of intracellular calcium

Kozaki, Yasuko; Kambe, Fukushi; Hayashi, Yoshitaka; Ohmori, Sachiko; Seo, Hisao; Kumazawa, Takao; Mizumura, Kazue

doi:10.1111/j.1471-4159.2006.04320.x

Cited by 14 publications

(12 citation statements)

References 45 publications

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“…U-73433 (10 À6 mol l À1 ), a negative analog of U-73122, 20 showed no effect (Figures 2b and e, n ¼ 8). On the other hand, inhibition of protein kinase A or phospholipase A 2 with H-89 (10 À6 mol l À1 , n ¼ 5) 8,23 or AACOCF 3 (3 Â 10 À5 mol l À1 , n ¼ 8), 29 respectively, did not alter the effects of bradykinin (Figures 2c-e).…”

Section: Resultsmentioning

confidence: 92%

“…The following drugs were used: bradykinin (10 À7 mol l À1 ), 3 U-73122 (10 À6 mol l À1 ), 20 U-73433 (10 À6 mol l À1 ), 20 cyclopiazonic acid (3 Â 10 À6 mol l À1 ), 21 HC-030031 (5 Â 10 À6 mol l À1 ), 22 H-89 (10 À6 mol l À1 ), 8,23 XE-991 (10 À5 mol l À1 ), 24 bisindolylmaleimide-I (10 À6 mol l À1 ), 25 capsaicin (10 À5 mol l À1 ), 26 capsazepine (5 Â 10 À6 mol l À1 ) 27 and phentolamine (10 À4 mol l À1 ) 28 from Sigma-Aldrich (St Louis, MO, USA) arachidonyl trifluoromethyl ketone (3 Â 10 À5 mol l À1 , AACOCF 3 ) 29 from Calbiochem (San Diego, CA, USA) o-conotoxin GVIA (2 Â 10 À9 or 10 À6 mol l À1 ) 30,31 and Calcitonin Gene-Related Peptide (Human, 8-37) (CGRP8-37, 10 À7 mol l À1 ) 32 from Peptide Institute (Osaka, Japan) and wortmannin (10 À5 mol l À1 ) 33 and AP-18 (10 À6 mol l À1 ) 34 from Biomol (Plymouth Meeting, PA, USA). Stock solutions of bradykinin, phentolamine, oconotoxin GVIA, H-89 and CGRP8-37 were dissolved in distilled water.…”

Section: Drugsmentioning

confidence: 99%

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Facilitation of sympathetic neurotransmission by phosphatidylinositol-4,5-bisphosphate-dependent regulation of KCNQ channels in rat mesenteric arteries

et al. 2012

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Sympathetic nerves regulate vascular tone by releasing neurotransmitters into the vasculature. We previously demonstrated that bradykinin facilitates sympathetic neurotransmission in rat mesenteric arteries. Although little is known about the intracellular mechanism modulating this neurotransmission, recent cell line experiments have shown that the KCNQ channel, which is inhibited by the depletion of membrane phosphatidylinositol-4,5-bisphosphate (PIP 2 ), participates in the control of neurotransmission by bradykinin. In the present study, we examined the mechanism regulating neurotransmitter release from rat perivascular sympathetic nerves. Excitatory junction potentials (EJPs) elicited by repetitive nerve stimulation (1 Hz, 11 pulses, 20 ls, 20-50 V), a measure of sympathetic purinergic neurotransmission, were recorded with a conventional microelectrode technique in rat mesenteric arteries. Bradykinin (10 À7 mol l À1 ) significantly enhanced the amplitude of EJPs (n ¼ 22, Po0.05). This enhancing effect was abolished by N-type calcium-channel inhibition with x-conotoxin GVIA (2 Â 10 À9 mol l À1 , n ¼ 8). The blockade of phospholipase C with U-73122 (10 À6 mol l À1 , n ¼ 17) also eliminated the facilitatory effect of bradykinin. In addition, the effects of bradykinin were diminished by the prevention of PIP 2 resynthesis with wortmannin (10 À5 mol l À1 n ¼ 7) or KCNQ channel inhibition with XE-991 (10 À5 mol l À1 , n ¼ 7). On the other hand, depletion of intracellular calcium stores with cyclopiazonic acid (3 Â 10 À6 mol l À1 , n ¼ 6) or the inhibition of protein kinase C with bisindolylmaleimide-I (10 À6 mol l À1 , n ¼ 9) did not alter the action of bradykinin. These data demonstrate that the hydrolysis of PIP 2 by phospholipase C, which is activated by G q/11 -coupled receptors, and subsequent KCNQ channel inhibition enhance sympathetic purinergic neurotransmission presumably via the activation of N-type calcium channels in rat mesenteric arteries.

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Section: Resultsmentioning

confidence: 92%

Section: Drugsmentioning

confidence: 99%

Facilitation of sympathetic neurotransmission by phosphatidylinositol-4,5-bisphosphate-dependent regulation of KCNQ channels in rat mesenteric arteries

et al. 2012

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“…Later, EP 3A receptors were cloned from dog DRG neurons and shown to couple with G i and G q protein (385). In rat trigeminal ganglion, significant EP 2 , EP 3 , and EP 4 receptor expression was observed along with a lower density of EP 1 receptors (521).…”

Section: Prostanoid Receptors and Their Intracellular Signaling Mechamentioning

confidence: 99%

“…In a heterologous expression system containing the EP 3 (EP 3A or EP 3B ) plus B 2 receptors, an agonist of EP 3 receptors restored the second, desensitized, bradykinin response (mobilization of intracellular Ca 2ϩ ) without modifying the greater first response, i.e., it diminished B 2 receptor tachyphylaxis (385). Surprisingly, this effect of EP 3 receptor stimulation was mediated by the G i protein and consequent reduction of PKA activity in case of both EP 3A or EP 3B receptors.…”

Section: Prostanoid-induced Sensitization To Chemical Stimulimentioning

confidence: 99%

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

Pethő

Reeh

2012

Physiological Reviews

240

200

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Peripheral mediators can contribute to the development and maintenance of inflammatory and neuropathic pain and its concomitants (hyperalgesia and allodynia) via two mechanisms. Activation or excitation by these substances of nociceptive nerve endings or fibers implicates generation of action potentials which then travel to the central nervous system and may induce pain sensation. Sensitization of nociceptors refers to their increased responsiveness to either thermal, mechanical, or chemical stimuli that may be translated to corresponding hyperalgesias. This review aims to give an account of the excitatory and sensitizing actions of inflammatory mediators including bradykinin, prostaglandins, thromboxanes, leukotrienes, platelet-activating factor, and nitric oxide on nociceptive primary afferent neurons. Manifestations, receptor molecules, and intracellular signaling mechanisms of the effects of these mediators are discussed in detail. With regard to signaling, most data reported have been obtained from transfected nonneuronal cells and somata of cultured sensory neurons as these structures are more accessible to direct study of sensory and signal transduction. The peripheral processes of sensory neurons, where painful stimuli actually affect the nociceptors in vivo, show marked differences with respect to biophysics, ultrastructure, and equipment with receptors and ion channels compared with cellular models. Therefore, an effort was made to highlight signaling mechanisms for which supporting data from molecular, cellular, and behavioral models are consistent with findings that reflect properties of peripheral nociceptive nerve endings. Identified molecular elements of these signaling pathways may serve as validated targets for development of novel types of analgesic drugs.

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“…Intracellular ROS were measured by a fluorescent dye technique (Kozaki et al 2007). MIN6 cells were cultured on glass cover slips and were treated for 30 min with 20 μM 2′,7′-dichlorofluorescin diacetate (H2DCFDA, Molecular Probes) in phosphate buffered saline.…”

Section: Measurement Of Cellular Ros Productionmentioning

confidence: 99%

Cholesterol induces pancreatic β cell apoptosis through oxidative stress pathway

Liu

Hou

et al. 2011

Cell Stress and Chaperones

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Type 2 diabetes is often associated with high blood cholesterol. Here, we investigated the effect of cholesterol loading on MIN6 cells derived from pancreatic β cells. Exposure of MIN6 cells to cholesterol-induced apoptosis in time-and dose-dependent manner. Treatment with methyl-β-cyclodextrin that removes cholesterol from plasma membrane prevented the cells from cholesterolinduced apoptosis. Western blot analysis revealed that the levels of phosphorylated-p38 mitogen-activated protein kinase (P-p38 MAPK) and c-Jun N-terminal kinases (P-JNK) were significantly increased after the cholesterol loading, suggesting that the stress-activated protein kinase signaling was stimulated. A specific p38 inhibitor rescued MIN6 cells from cholesterol-induced apoptosis, while JNK inhibitor failed, suggesting the importance of activation of p38 MAPK signaling in response to cholesterol. The expression of Bip and CHOP, the endoplasmic reticulum (ER) stress markers, remained unaffected, indicating that the ER stress may not be involved in the cytotoxicity of cholesterol on the MΙΝ6 cells. The intracellular concentration of reactive oxygen species measured by use of 2′,7′-dichlorofluorescin diacetate was significantly increased after cholesterol loading, demonstrating the induced apoptosis was mediated through oxidative stress. Addition of reduced form of glutathione in the medium rescued MIN6 cells from apoptosis induced by cholesterol loading. Taken together, these results demonstrate that the free cholesterol loading can induce apoptosis of MIN6 cells mediated by oxidative stress and the activation of p38 MAPK signaling.

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Molecular cloning of prostaglandin EP3 receptors from canine sensory ganglia and their facilitatory action on bradykinin‐induced mobilization of intracellular calcium

Cited by 14 publications

References 45 publications

Facilitation of sympathetic neurotransmission by phosphatidylinositol-4,5-bisphosphate-dependent regulation of KCNQ channels in rat mesenteric arteries

Facilitation of sympathetic neurotransmission by phosphatidylinositol-4,5-bisphosphate-dependent regulation of KCNQ channels in rat mesenteric arteries

Sensory and Signaling Mechanisms of Bradykinin, Eicosanoids, Platelet-Activating Factor, and Nitric Oxide in Peripheral Nociceptors

Cholesterol induces pancreatic β cell apoptosis through oxidative stress pathway

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