Pertussis toxin stimulates delayed‐onset, Ca2+‐dependent catecholamine release and the ADP‐ribosylation of a 40 kDa protein in bovine adrenal chromaffin cells

Brocklehurst, Keith; Pollard, Harvey B.

doi:10.1016/0014-5793(88)80133-9

Cited by 20 publications

(11 citation statements)

References 23 publications

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“…We report for the first time that long-term (8 or 24 h) treatment of BAMC cells with pertussis toxin caused a pronounced concentration-and time-dependent increase in ME secretion. The results of our short-term (1 h) study are in agreement with the report by Broklehurst and Pollard [6] in that the effect of short-term pertussis toxin on catechol amine secretion was weak. However, in the present study we found that long-term stimu lation (8 or 24 h) of BAMC cells with pertussis toxin caused a pronounced stimulation of ME secretion, suggesting that pertussis toxin-sen sitive G proteins play an important role in the regulation of the long-term secretion of ME in BAMC cells.…”

Section: Discussionsupporting

confidence: 83%

“…Pertussis toxin-induced ADP-ribosylation of the 40-kDa protein in BAMC cells and catecholamine release are correlated [3,6], Thus the pronounced increase in ME secre tion by pertussis toxin after 8 and 24 h in our study could be due to ADP-ribosylation. In creases of secretion of ME induced by pertus sis toxin are probably not due to its toxic effect since the concentration of pertussis toxin used in the present study does not cause the release of endogenous lactate dehydroge nase, indicating that the cells remained intact during incubation with pertussis toxin [6], To find the mechanisms involved in per tussis toxin-induced responses, the interac tion of pertussis toxin with different second messenger systems was studied. Our results suggest that the influx of calcium is required for both the increased secretion of ME and the enhanced expression of proENK mRNA in duced by pertussis toxin.…”

Section: Discussionmentioning

confidence: 66%

“…in a delayed manner [5,6] and potentiated the catecholamine release induced by several secretagogues such as acetylcholine, nicotine, histamine, and KC1 in BAMC cells [3. 7].…”

Section: Exposure Of Bovine Adrenal Medullary Chromaffin (Bamc) Cellsmentioning

confidence: 99%

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Pertussis Toxin Stimulates the Secretion of [Met5]-Enkephalin and the Expression of Proenkephalin A mRNA in Bovine Adrenal Medullary Chromaffin Cells

Suh¹,

Hudson²,

McMillian³

et al. 1992

Biological Signals

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[Met⁵]-Enkephalin (ME) secretion and the expression of proenkephalin A (proENK) mRNA were studied following long-term exposure of bovine adrenal medullary chromaffin (BAMC) cells to pertussis toxin. Treatment with pertussis toxin for 24 h increased the secretion of ME in a concentration- and time-dependent manner. The magnitude of ME secretion continued to increase with time in the presence of pertussis toxin. The intracellular concentration of ME in the pertussis toxin-treated group was not significantly different from controls, suggesting that elevated levels of ME secretion result from increased biosynthesis of ME rather than from release of stored ME. Prolonged (24 h) stimulation of BAMC cells with pertussis toxin also increased proENK gene expression. Pretreatment with nimodipine (a calcium channel blocker) and calmidazolium (a calmodulin antagonist) inhibited both the secretion of ME and the increase in proENK mRNA levels induced by pertussis toxin, while the intracellular calcium antagonist dantrolene and the protein kinase C inhibitors sphingosine and H7 [1-(5-isoquinolinylsulfonyl)-2-methylpiperazine] were ineffective in blocking pertussis toxin-induced responses. Forskolin (an adenyl cyclase activator) and isobutyl methyl xanthine (a phosphodiesterase inhibitor) increased both ME secretion and proENK mRNA levels; pertussis toxin synergistically increased the secretion of ME with these cyclic AMP-elevating agents but had only an additive effect with these agents on the level of proENK mRNA. Our results suggest that a pertussis toxin-sensitive G protein may tonically regulate the secretion of ME as well as the level of proENK mRNA. Calcium influx and calmodulin, but not protein kinase C and cyclic AMP, appeared to be the major second messengers involved in these pertussis toxin-induced responses.

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Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 66%

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Pertussis Toxin Stimulates the Secretion of [Met5]-Enkephalin and the Expression of Proenkephalin A mRNA in Bovine Adrenal Medullary Chromaffin Cells

Suh¹,

Hudson²,

McMillian³

et al. 1992

Biological Signals

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“…Pertussis toxin stimulates CA release from cultured bovine chromaffin cells in the absence of any exoge-nous stimulatory or inhibitory agonists for this cell (Brocklehurst & Pollard, 1988). The effect of the toxin was only apparent after an approximately 2 hr time lag, although exposure times as short as 15 min were sufficient for the effect of the toxin to develop.…”

Section: Introductionmentioning

confidence: 99%

Pertussis toxin stimulation of catecholamine release from adrenal medullary chromaffin cells: Mechanism may be by direct activation of L-type and G-type calcium channels

et al. 1991

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We have previously shown that pertussis toxin (PTX) stimulates delayed-onset, [Ca2+]o-dependent catecholamine (CA) release from bovine chromaffin cells. We now show that this effect of PTX is inhibited in part (50%) by dihydropyridine Ca(2+)-channel antagonists niludipine and nifedipine, and is potentiated by the dihydropyridine Ca(2+)-channel agonist Bay K-8644. We and others have shown that pretreatment of chromaffin cells with PTX results in enhanced catecholamine secretion in response to high [K+]o, nicotine and muscarine, and here we extend these observations by showing that toxin pretreatment also enhances the secretory response to [Ba2+]o. All these data are consistent with the concept that PTX may act on Ca2+ channels. To examine the possibility of a direct action of the toxin on the voltage-gated L-type Ca2+ channel known to be present in these cells, we studied the effects of the toxin on whole cell Ca2+ currents. We found and report here that spontaneous electrical activity was considerably increased in PTX-treated cells. Our measurements of whole cell inward Ca2+ currents indicate that the underlying mechanism is a marked shift of the activation curve of the L-type Ca2+ current along the voltage axis towards more negative potentials. While treatment of the cells with PTX had no effect on L-type Ca(2+)-channel conductance (6 nS/cell at 2.6 mM [Ca2+]o). PTX evoked the activation of a new class of Ca(2+)-selective channels (5 pS in 25 mM [Ca2+]pipet), which are rather insensitive to membrane potential.(ABSTRACT TRUNCATED AT 250 WORDS)

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“…Several laboratories have reported that pretreatment of chromaffin cells with pertussis toxin (PTX) enhances both basal secretion from those cells and secretion in response to secretagogues including acetylcholine, nicotine, muscarinic agonists, and elevated K+ (Tanaka et al, 1987;Brocklehurst and Pollard, 1988;Ohara-Imaizumi et al, 1988, 1990Sasakawa et al, 1988;O'Sullivan and Burgoyne, 1989;Bansal et al, 1990;Sontag et al, 1991). Although three G-protein substrates for PTX-catalyzed ADP ribosylation have been identified in chromaffin cells (Toutant et al, 1987), the mechanism by which PTX produces this secretion-enhancing effect is unclear.…”

mentioning

confidence: 99%

Pertussis Toxin Enhances Proenkephalin Synthesis in Bovine Chromaffin Cells

Wilson¹

1993

Journal of Neurochemistry

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The synthesis of the neuropeptide precursor proenkephalin was measured in bovine adrenal chromaffin cells following radiolabeling with [35S]methionine. Treatment of chromaffin cells with pertussis toxin (100 ng/ml) approximately doubled proenkephalin synthesis without altering total protein synthesis. Pertussis toxin pretreatment also increased proenkephalin synthesis in chromaffin cells exposed to vasoactive intestinal peptide (VIP) and 3-isobutyl-1-methylxanthine (IBMX). Combinations of IBMX plus nicotine, VIP, or histamine also synergistically enhanced proenkephalin synthesis, with no further elevation when the cells were also pretreated with pertussis toxin. The action of forskolin, a direct activator of adenylate cyclase, on proenkephalin synthesis was similarly potentiated by pertussis toxin or IBMX, presumably reflecting the abilities of both the toxin and this phosphodiesterase inhibitor to enhance the cyclic AMP response to forskolin. In contrast, increased synthesis of proenkephalin in response to phorbol esters was not affected by pertussis toxin treatment. These results suggest that pertussis toxin potentiates proenkephalin synthesis primarily through inactivation of guanine nucleotide-binding proteins that inhibit adenylate cyclase, although other signaling pathways may also be involved.

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Pertussis toxin stimulates delayed‐onset, Ca²⁺‐dependent catecholamine release and the ADP‐ribosylation of a 40 kDa protein in bovine adrenal chromaffin cells

Cited by 20 publications

References 23 publications

Pertussis Toxin Stimulates the Secretion of [Met<sup>5</sup>]-Enkephalin and the Expression of Proenkephalin A mRNA in Bovine Adrenal Medullary Chromaffin Cells

Pertussis Toxin Stimulates the Secretion of [Met<sup>5</sup>]-Enkephalin and the Expression of Proenkephalin A mRNA in Bovine Adrenal Medullary Chromaffin Cells

Pertussis toxin stimulation of catecholamine release from adrenal medullary chromaffin cells: Mechanism may be by direct activation of L-type and G-type calcium channels

Pertussis Toxin Enhances Proenkephalin Synthesis in Bovine Chromaffin Cells

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