Endothelin‐Mediated Calcium Response and Inositol 1,4,5‐Trisphosphate Release in Neuroblastoma‐Glioma Hybrid Cells (NG108‐15): Cross Talk with ATP and Bradykinin

Chau, Lee‐Young; Lin, Teng Nan; Chang, Wen Tsan; Chen, C.-H.; Shue, M.-J.; Hsu, Yu-Shen; Hu, C.-Y.; Tsai, Wen-Hsuan; Sun, Grace Y.

doi:10.1111/j.1471-4159.1993.tb03172.x

Cited by 17 publications

(5 citation statements)

References 40 publications

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“…Our results are compatible with previous reports on ET stimulation of PIs turnover in rat neuroblastoma-glioma hybrid cells (Chau et al, 1993), glial cells (Marsault et al, 1990), in cerebellar granule and glioma cells , and in brain structures such as the subfornical organ and median eminence (Garrido and Israel, 1994). Our findings differ from the previous study of bovine chromaffin ETs-stimulated cGMP production (right) in rat adrenal medulla.…”

Section: Discussioncontrasting

confidence: 56%

Endothelin Signaling Pathways in Rat Adrenal Medulla

Israel¹,

Mathison

Rosario³

2006

Cell Mol Neurobiol

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1. We further characterized the effect of endothelins (ETs) on receptor-mediated phosphoinositide (PI) turnover, nitric oxide synthase (NOS) activation, and cGMP formation in whole rat adrenal medulla. 2. The PI hydrolysis was assessed as accumulation of inositol monophosphates (InsP(1)) in the presence of 10 mM LiCl in whole tissue and the analysis of inositol-1-phosphate by Dowex anion exchange chromatography. NOS activity was assayed by monitoring the conversion of radiolabeled L-arginine to L-citrulline. Cyclic GMP formation was assessed as accumulation of cGMP in whole tissue in the presence of phosphodiesterase inhibition, and the amount of cGMP formed was determined by radioimmuno-antibody procedure. 3. ET-1 and ET-3 increased PI turnover by 30% in whole adrenal medulla prelabeled with [(3)H] myoinositol. Both ETs isoforms, at equimolar doses, increased NOS activity and cGMP levels in similar degree. The selective ET(B) receptor agonist, IRL-1620, also increased cGMP formation, mimicking the effects of ETs, while IRL-1620 did not alter the PI metabolism. ETs-induced InsP(1) accumulation and cGMP was dependent on extracellular calcium. The effect of ETs on PI turnover was inhibited by neomycin. The L-arginine analogue, N-nitro-L-arginine (L-NAME), and two inhibitors of soluble guanylyl cyclase, methylene blue and ODQ, significantly inhibited the increase in cGMP production induced by ETs or IRL-1620. The selective ET(A) receptor antagonist, BQ 123, inhibited the ETs-induced increase in PI turnover, while the selective ET(B) receptor antagonist, BQ 788, was ineffective. Likewise, BQ 788, significantly inhibited ET-1- or ET-3-induced NOS activation and cGMP generation but not ETs-induced InsP(1) accumulation. 4. Our data indicate that stimulation of PI turnover and NO-induced cGMP generation constitutes ETs signaling pathways in rat adrenal medulla. The former action is mediated through activation of ET(A) receptor, while the latter through the activation of ET(B) receptor. These results support the role of endothelins in the regulation of adrenal medulla function.

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Section: Discussioncontrasting

confidence: 56%

Endothelin Signaling Pathways in Rat Adrenal Medulla

Israel¹,

Mathison

Rosario³

2006

Cell Mol Neurobiol

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“…The high capacity of bradykinin to induce desensitization processes is emphasised by the finding that bradykinin can also very efficiently induce heterologous desensitization. Recently it was reported that bradykinin completely abolishes the endothelin-induced cytosolic [Ca"] rise in NG 108-15 cells (Chau et al, 1993).…”

Section: Properties Of the Nuclear [Ca2+] Risementioning

confidence: 99%

Bradykinin induces rise of free calcium in nuclei of neuroblastoma × glioma hybrid NG 108‐15 cells

Beckmann¹,

Lindschau

Haller

1995

J of Neuroscience Research

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Confocal fluorescence microscopy was used to study the bradykinin-induced calcium signals in the neuroblastoma x glioma cell line NG 108-15. We found that bradykinin induced a rise in free calcium, not only in the cytoplasm but also in the nucleus. The nuclear and cytosolic calcium concentrations were not significantly different and rose to about 1.2 microM. The signal was mediated by the B2-receptor subtype as confirmed using the specific antagonist Hoe 140. Both the onset and the intensity of the calcium signals were concentration-dependent. The rise of nuclear calcium level was independent of extracellular calcium and suppressed by thapsigargin which is known to deplete inositol 1,4,5-trisphosphate-sensitive calcium stores. Bradykinin-induced calcium increase desensitizes rapidly. This desensitization was shown not to involve activation of protein kinase C.

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“…For example, ET facilitates the release of intracellular Ca2" with a slow equilibrium with the extracellular cation in contrast to the Ca2" pool mobilized by ATP (Figure 7a). In this connection, Chau et al (1993) recently suggested that both ET and ATP hydrolyze a separate pool of polyphosphoinositides in neuroblastoma-glioma hybrid cells resulting in additive responses due to the release of separate pools of Ca2+. Alternatively, an ETA membrane receptor may 'cross-talk' with a P2.-purinoceptor increasing its affinity and/or modifying its ionophore function ( Figure 7b).…”

Section: Discussionmentioning

confidence: 99%

“…For example, ET facilitates the release of intracellular Ca2" with a slow equilibrium with the extracellular cation in contrast to the Ca2" pool mobilized by ATP (Figure 7a). In this connection, Chau et al (1993) creasing its affinity or altering the kinetics of its ionophore function (Figure 7c). With regard to the increase in bladder tension caused by the ETs, the ETA receptor involved could be coupled to a calcium channel mainly dependent on the influx of extracellular Ca2+ (Figure 7).…”

Section: Discussionmentioning

confidence: 99%

Involvement of ET_A receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder

Donoso

Salas

Sepulveda

et al. 1994

British J Pharmacology

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1 Endothelin-1 (ET-1; 3-10 nM) raised the tone of rat bladders bathed in buffer containing atropine (1 gtM) plus guanethidine (3.4 JAM). In addition, ET-1 potentiated, in a concentration-dependent fashion (1-10 nM), the contractions evoked by both transmural nerve stimulation and applications of exogenous adenosine 5'-triphosphate (ATP). 2 The threshold concentration of ET-1 required to facilitate non-adrenergic non-cholinergic (NANC) transmission and potentiate ATP-induced contractions, was about 10 fold lower than that required to increase the bladder tone (3 nM). 3 The ET-1-induced increase in basal tension reached its maximal effect within 60-90 s. In contrast, the 7.8 JAM ATP-induced contractions increased by 50% within the first minute following incubation with 1O nM ET-1 but required about 5 min to develop the maximal effect. 4 The ET-1-induced potentiation of NANC or ATP responses was long-lasting and persisted in spite of extensive washing. The recovery of the bladder excitability depended on the concentration of ET-1. Following the application of 3 nM ET-1, recovery required 30 min; applications of 10 nM ET-1 required at least 60 min for full recovery. 5The ET-1-induced potentiation of responses was selective for ATP and related structural analogues.ET-1 did not modify the contractions induced by acetylcholine, 5-hydroxytryptamine, prostaglandin F2, or bradykinin. 6 The potency of ET-2 was similar to that of ET-1. ET-3 and ET-C-terminal hexapeptide were inactive up to 100 M. Sarafotoxin S6b was 2 to 3 fold less potent than ET-1 whereas sarafotoxin S6c (100 nM) was inactive. AGETB-9 and AGETB-89, two ETB receptor agonists, were also inactive (up to 100 nM). 7 Removal of one or both disulphide bonds in ET-1 and tryptophan-21 formylation of ET-1, resulted in inactive peptides (up to 100 nM). 8 The ET-1 receptor antagonists, BE-18257B and FR 139317, blocked both the ET-1-induced rise in tone and the potentiation of ATP responses in a concentration-dependent fashion. FR 139317 was at least 30 fold more potent than BE-18257B. Both antagonists blocked at lower concentrations the ET-l increase in bladder tone as compared to the ATP potentiation. The antagonism was slowly reversible. 9 Results are consistent with the presence of ETA receptors in the rat bladder, which mediate both actions of ET-1. The interaction of ET-1 with purinergic mechanisms is discussed.

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Endothelin‐Mediated Calcium Response and Inositol 1,4,5‐Trisphosphate Release in Neuroblastoma‐Glioma Hybrid Cells (NG108‐15): Cross Talk with ATP and Bradykinin

Abstract: J. Neurochem. 60,[454][455][456][457][458][459][460].

Cited by 17 publications

References 40 publications

Endothelin Signaling Pathways in Rat Adrenal Medulla

Endothelin Signaling Pathways in Rat Adrenal Medulla

Bradykinin induces rise of free calcium in nuclei of neuroblastoma × glioma hybrid NG 108‐15 cells

Involvement of ET_A receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder

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Endothelin‐Mediated Calcium Response and Inositol 1,4,5‐Trisphosphate Release in Neuroblastoma‐Glioma Hybrid Cells (NG108‐15): Cross Talk with ATP and Bradykinin

Abstract: J. Neurochem. 60,[454][455][456][457][458][459][460].

Cited by 17 publications

References 40 publications

Endothelin Signaling Pathways in Rat Adrenal Medulla

Endothelin Signaling Pathways in Rat Adrenal Medulla

Bradykinin induces rise of free calcium in nuclei of neuroblastoma × glioma hybrid NG 108‐15 cells

Involvement of ETA receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder

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Product

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Involvement of ET_A receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder