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Z J Cui

Publications and source records attributed to Z J Cui.

17 recordsLinked to original sources
PubMed2001

Nitrate respiratory metabolism in an obligately autotrophic hydrogen-oxidizing bacterium, Hydrogenobacter thermophilus TK-6.

Hydrogenobacter thermophilus strain TK-6 was observed to grow anaerobically on nitrate as an electron acceptor when molecular hydrogen was used as an energy source. Nitrite was detected as the product of a respiratory reaction. 15NO, 15N2O, and 15N2 were detected with Na15NO3 as an electron acceptor. Western immunoblot analysis showed that cell-free extracts from cells grown on nitrate reacted with antibodies against heme cd1-type nitrite reductase from Pseudomonas aeruginosa. The positive bands, which had molecular masses similar to that of the heme cd1-type nitrite reductase, were also stained by heme staining. These results indicate that nitrite reductase of strain TK-6 is a heme cd1-type enzyme. Activity of ATP:citrate lyase, one of the key enzymes of the reductive TCA cycle, was detected in cell-free extract of cells cultivated on nitrate, which indicates that the cycle operates during anaerobic growth.

Adenosine Triphosphate↗
PubMed2000

Photodynamic modulation of adrenergic receptors in the isolated rat hepatocytes.

In isolated rat hepatocytes, noradrenaline (NA) 50 nM induced intracellular calcium ([Ca(2+)](c)) increase as (i) oscillations with each down-stroke of the spike reaching baseline, (ii) phasic increase with gradual decay, and (iii) phasic increase transforming into oscillations. At 25 nM and 50 nM, NA predominantly induced oscillatory increases; at 100 nM and 1 microM, phasic increases were predominant. Photodynamic action (30 s) with photosensitizer sulphonated aluminium phthalocyanine (SALPC, 5 microM) induced [Ca(2+)](c) increase as (i) no change, (ii) a single spike, or (iii) phasic increase. [Ca(2+)](c) oscillations induced by NA 50 nM were obliterated by photodynamic action (30 s), but when NA 200 nM, which normally induced plateau increases, was added to the now quiescent cells, [Ca(2+)](c) oscillations reemerged. These data indicate that photodynamic action could efficiently desensitize adrenergic receptors in hepatocytes. Photodynamic action may do so by crosslinking neighboring receptors or neighboring transmembrane domains of the same receptor.

Adrenergic alpha-Agonists↗
PubMed2000

Cholecystokinin analog JMV-180-induced intracellular calcium oscillations are mediated by inositol 1,4,5-trisphosphate in rat pancreatic acini.

AIM: To investigate whether inositol 1,4,5-trisphosphate (IP3) is involved in secretory response of pancreatic acini to cholecystokinin (CCK) analog Boc-Tyr (SO3H)-Nle-Gly-Trp-Nle-Asp-2-phenylethylester.2NH3 (JMV-180). METHODS: Dynamics of cytosolic Ca2+ concentration, [Ca2+]c, was recorded by ratiometry of Fura-2 in pancreatic acini. RESULTS: In perfused preparations of isolated rat pancreatic acinar cells, 2-aminoethoxydiphenylborate (2APB), a new membrane permeant inhibitory modulator of IP3-mediated calcium release from internal stores, inhibited JMV-180-induced [Ca2+]c spikes, and 2APB at 100 mumol.L-1 resulted in an immediate, complete inhibition of the spikes. CONCLUSION: Recurrent [Ca2+]c spikes induced by continuous stimulation with JMV-180 are initiated via IP3-mediated Ca2+ release from internal Ca2+ stores.

Animals↗
PubMed1998

Types of voltage-dependent calcium channels involved in high potassium depolarization-induced amylase secretion in the exocrine pancreatic tumour cell line AR4-2J.

In the perifused fura-2 loaded exocrine pancreatic acinar cell line AR4-2J pulses of high potassium induced repetitive increases in intracellular calcium. Attached cells when stimulated with high potassium secreted large amount of amylase. High potassium-induced secretion was dependent both on the concentration of potassium and duration of stimulation. High potassium induced increases in intracellular calcium were inhibited by voltage-dependent calcium channel antagonists with an order of potency as follows: nifedipine > omega-agatoxin IVA > omega-conotoxin GVIA. In contrast, the L-type calcium channel antagonist nifedipine almost completely inhibited potassium-induced amylase secretion, whereas the N-type channel antagonist omega-conotoxin GVIA was without effect. The P-type channel antagonist omega-agatoxin IVA had a small inhibitory effect, but this inhibition was not significant at the level of amylase secretion. In conclusion, the AR4-2J cell line possesses different voltage-dependent calcium channels (L, P, N) with the L-type predominantly involved in depolarization induced amylase secretion.

Amylases↗
PubMed1998

Photodynamic modulation of cellular function.

Photodynamic action with a large number of photosensitisers has important practical implications such as photodynamic cancer therapy. But the cellular and molecular mechanisms involved have been rather poorly understood. In this paper, photodynamic modulation of cell signal transduction and the resultant changes in cellular function are reviewed, with a particular emphasis on smooth muscle and the pancreas.

Animals↗
PubMed1997

Photodynamic triggering of calcium oscillation in the isolated rat pancreatic acini.

1. Photodynamic agents, due to their photon-dependent selective activation, can selectively activate a number of physiological processes and may directly modulate signal transduction in a number of cells including pancreatic acinar cells. 2. Activation of the photodynamic agent sulphonated aluminium phthalocyanine (SALPC) triggered recurrent cytosolic calcium ([Ca2+]i) spiking in pancreatic acinar cells. 3. The photodynamically triggered calcium spiking could be blocked by phosphatidylinositol-specific phospholipase C (PI-PLC) inhibitor U73122, but not by phosphatidylcholine-specific phospholipase C inhibitor D609. 4. Removal of extracellular Ca2+ abolished spiking, as did 2-aminoethoxydiphenylborate (2-APB), an inhibitory modulator of IP3-mediated Ca2+ release from intracellular stores. 5. These data suggest that SALPC photodynamic action may permanently fix PI-PLC in an active conformation, and this produced recurrent [Ca2+]i spiking.

Animals↗
PubMed1997

A novel aspect of photodynamic action: induction of recurrent spikes in cytosolic calcium concentration.

Effects of photodynamic action of gadolinium porphyrin-like macrocycle B (PLMGdB) on cytosolic Ca2+ concentration, [Ca2+]c, was investigated in isolated rat pancreatic acini. The PLMGdB alone or light alone (2 min) had no effect on [Ca2+]c. Cell-bound PLMGdB upon brief (0.5-2.0 min) light activation triggered recurrent spikes in [Ca2+]c. At lower PLMGdB concentration (100 nM) the spikes continued during the whole period of monitoring [Ca2+]c. At a higher concentration of 500 nM, the spikes continued for the first 40 min, followed by a gradual increase in basal [Ca2+]c upon which smaller spikes were superimposed. At 1 microM, the spikes continued for the first 20 min, after that spiking gradually degenerated into a plateau phase. In many aspects, photodynamically triggered spikes resembled spikes generated by physiological concentrations of cholecystokinin. The spikes triggered by photodynamic action were likely to be the result of the ignition of a physiological "chain reaction", because functional inositol-1,4,5-trisphosphate (IP3) receptors were required for spiking to occur. Two-aminoethoxydiphenylborate, an inhibitory modulator of IP3-triggered Ca2+ release from intracellular stores, effectively inhibited photodynamically generated spikes. Therefore photodynamic action appears to be able to permanently transfix a physiological process, leading to long-lasting pharmacological or therapeutic effects.

Animals↗
PubMed1997

Muscarinic stimulation of calcium/calmodulin-dependent protein kinase II in isolated rat pancreatic acini.

AIM: To study whether M3 receptor occupation would lead to activation of calcium/calmodulin-dependent protein kinase II (CaM kinase II). METHODS: In this study, we isolated rat pancreatic acini by collagenase digestion; measured the Ca2+/calmodulin-independent activity of autophosphorylated form of the CaM kinase II both before and after stimulation of the acini with muscarinic secretagogue bethanechol (Bet). RESULTS: Bet stimulated the activation of, or generation of Ca(2+)-independent activity of, this kinase, in a concentration (0.0001-1 mmol.L-1) and time (5-300 s)-dependent manner; with Bet of 100 mumol.L-1, Ca(2+)-independent activity increased from an unstimulated level of 4.5 +/- 0.3 (n = 4) to 8.9 +/- 1.3 (n = 4, P < 0.05) at 5 s. Another Ca2+ mobilizing secretagogue cholecystokinin (CCK) also activated the kinase; at 1 mumol.L-1, CCK increased Ca(2+)-independent kinase activity to 12.9 +/- 0.5 (n = 6, P < 0.05). Vasoactive intestinal peptide (VIP) at 1 mumol.L-1 did not produce significant Ca(2+)-independent kinase activity (from control 3.90 +/- 0.28 to 4.53 +/- 0.47, n = 6, P > 0.05). Atropine completely blocked Bet activation of the kinase. CONCLUSION: CaM kinase II plays a pivotal role in digestive enzyme secretion, especially during the initial phase of amylase secretion.

Animals↗
PubMed1996

KN-62, a calcium/calmodulin-dependent protein kinase II inhibitor, inhibits high potassium-stimulated prolactin secretion and intracellular calcium increases in anterior pituitary cells.

In isolated rat anterior pituitary cells, KN-62 (10 microM), an isoquinoline sulfonamide inhibitor of calcium/calmodulin-dependent protein kinase II, inhibited high KCl(50 milliM)-stimulated prolactin secretion almost completely, with an IC50 of 95 nM KN-62 inhibited TRH-induced prolactin secretion less effectively. KN-04, a compound that is over 100-fold less active in inhibiting purified calcium/calmodulin-dependent protein kinase II, also inhibited high KCl-stimulated prolactin secretion with an IC50 of 500 nM. KN-62 and KN-04 (10 microM) both inhibited high KCl-stimulated increases in intracellular Ca2+ concentrations. We conclude that KN-62 and KN-04 inhibit activation of voltage-dependent calcium channels in anterior pituitary cells either directly or indirectly.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1996

[Molecular mechanisms of exocytosis].

Biochemical and pharmacological characterization of small synaptic vesicle (SSV) membrane proteins and genetic studies of yeast secretion mutants led to the identification of an exocytotic fusion complex. The Sŏllner-Rothman SNARE hypothesis has led to remarkable progresses in the understanding of the molecular mechanisms of neurotransmitter release, endocrine and exocrine cell secretion.

Animals↗
PubMed1994

Calcium/calmodulin-dependent protein kinase-II activation in rat pituitary cells in the presence of thyrotropin-releasing hormone and dopamine.

PRL release from rat lactotrophs in response to TRH is Ca2+ dependent. TRH-induced PRL release is inhibited either after repeated pulses of TRH or in the presence of dopamine. TRH, however, generates increases in intracellular Ca2+ concentrations ([Ca2+]i) in both conditions. Calcium/calmodulin-dependent protein kinase-II (CaM kinase-II) is a ubiquitous enzyme implicated in secretion. To determine whether down-regulation of CaM kinase-II activity caused the lack of responsiveness to increases in [Ca2+]i, we measured the generation of calcium/calmodulin-independent kinase activity. Anterior pituitary cells contain a 50-kilodalton form of CaM kinase-II, determined by immunoblot, and the enzyme is in lactotrophs, determined by immunocytochemistry. TRH rapidly and transiently increased calcium/calmodulin-independent kinase activity; the increase was maximal by 15 sec and returned to basal by 2 min. When TRH pulses (1 microM, 15 sec) were applied every 10 min, each pulse caused an increase in calcium/calmodulin-independent kinase activity of similar magnitude, and the activity returned to basal values between pulses. Pretreatment of cells with dopamine (1 microM; 30 min) inhibited PRL release, but did not prevent the increase in calcium/calmodulin-independent kinase activity. These results indicate that TRH still activates CaM kinase-II when PRL release is inhibited. Dopamine and repeated pulses of TRH must inhibit PRL release at a site after the TRH-induced increase in [Ca2+]i and at a site other than CaM kinase-II.

Animals↗
PubMed1993

Photodynamic drug action on isolated rat pancreatic acini. Mobilization of arachidonic acid and prostaglandin production.

Chloro-aluminium phthalocyanine sulphonate (SALPC) when photon-activated generates singlet oxygen, elicits amylase release and causes plasma membrane permeabilization of pancreatic acinar cells (Matthews and Cui, Biochem Pharmacol 39: 1444-1457, 1990). Amylase release precedes membrane permeabilization suggesting that the initial release of amylase may be due to direct stimulation by singlet oxygen of secretagogue receptors or their coupled guanine nucleotide binding proteins (G-proteins) and effector systems including phospholipase A2 (PLA2). The aim of the experiments reported here was to establish the extent to which PLA2 activation, arachidonic acid mobilization, and prostaglandin production are involved in the photon-induced action of SALPC on dispersed, perifused acini isolated from the rat pancreas. The mobilization of arachidonic acid by a major secretory stimulant of pancreatic exocrine cells, cholecystokinin octapeptide, was also assessed: it produced a time- and concentration-dependent (10(-10)-10(-6) M) stimulation of arachidonic acid output from acini prelabelled with [1-14C]arachidonic acid. In contrast, the kinetics of arachidonic acid mobilization with photon-activated SALPC 1 microM, 4500 or 18,400 lux light intensity (lambda > 570 mm), was biphasic, an intensity-dependent stimulation being preceded by a more immediate initial inhibition of output. Light activation of SALPC and singlet oxygen generation may evoke the stimulatory phase of arachidonic acid release by an action on G-proteins, or by PLA2 activated directly, or via calcium influx, because NaF 20 mM, mellitin 2 mg/mL and the calcium ionophore A23187 1 microM caused a 2.9-, 33- and 5-fold increase, respectively, in arachidonic acid output. However, not only was the arachidonate stimulation delayed in response to SALPC but in other experiments designed to gain more insight into the turnover of arachidonic acid and its metabolites, the photodynamic release of amylase preceded maximum prostaglandin E2 (PGE2) output and amylase release was completely unaffected when PGE2 production was blocked by the cyclo-oxygenase inhibitor, indomethacin 10 microM. It is therefore likely that the rapid initial photodynamic release of amylase from pancreatic acini induced by SALPC is mediated by activation of the signal transduction pathway involving the release of intracellular calcium; arachidonic acid mobilization and prostanoid production may then be linked to the longer-term, cytolytic action of SALPC, especially in tumour cells.

Amylases↗
PubMed1992

Thyrotropin-releasing hormone-mediated Mn2+ entry in perifused rat anterior pituitary cells.

Receptor-mediated Ca2+ influx has been shown to exist in several cell types. Thyrotropin-releasing-hormone (TRH)-stimulated Ca2+ entry has also been postulated to exist in rat anterior pituitary cells, but direct evidence has been lacking. We have measured the fluorescence quenching of indo-1 caused by Mn2+ at a Ca(2+)-insensitive wavelength to investigate the actions of TRH on cation entry in dispersed perifused anterior pituitary cells. In indo-1-loaded cells perifused with Ca(2+)-free medium, Mn2+ caused fluorescence quenching in unstimulated cells; TRH caused further quenching. TRH-stimulated Mn2+ entry was transient, and levelled off within a few minutes in the presence of continuous TRH infusion. TRH-stimulated Mn2+ entry was dependent on the concentration of Mn2+ (50 microM-1 mM). TRH (1 microM) caused a larger effect than TRH (10 nM). La3+ and Ni2+ blocked the quenching stimulated by TRH. The rate of basal quenching was not blocked by dopamine, but TRH-stimulated Mn2+ entry was partially blocked by 1 microM-dopamine and almost completely abolished by 10 microM-dopamine. Thapsigargin (1-5 microM), a tumour promotor which depleted intracellular Ca2+ stores, had little effect on Mn2+. F- (20 mM), which activates G-proteins, also had little effect on Mn2+ entry. We conclude that TRH can transiently stimulate Ca2+ entry through a channel than can pass Mn2+ and be inhibited by dopamine. Depleting Ca2+ stores alone is not sufficient to stimulate Ca2+ entry, and so TRH must do so by other mechanisms.

Animals↗
PubMed1990

Photodynamic action of sulphonated aluminium phthalocyanine (SALPC) on isolated rat pancreatic acini.

The photodynamic action of SALPC has been investigated on dispersed, perifused, acini isolated from the rat pancreas. Stimulation of secretion was assessed by measuring amylase release and membrane permeabilization determined by the leakage of cytoplasmic lactate dehydrogenase (LDH) and by the efflux of 86Rb from preloaded acini. Light alone (greater than 570 nm, less than or equal to 18,400 lux), or SALPC (less than or equal to 1 microM) in the absence of light, had no effect on pancreatic acini but cellularly bound SALPC when illuminated caused a dose-dependent, light intensity-dependent and temperature-dependent release of amylase. Singlet oxygen generated by photon-activation of SALPC was measured by the formation of an imidazole adduct and bleaching of the secondary substrate, RNO. Whereas illumination caused a rapid increase in photodynamically-evoked pancreatic amylase release, the efflux of 86Rb and loss of cytosolic LDH were markedly delayed in onset: similar results were obtained with monochromatic laser light (633 nm). In contrast, the muscarinic agonist bethanechol evoked a rapid increase in amylase release but with an almost immediate efflux of 86Rb. Finally, electron microscopy confirmed that the structural integrity of the pancreatic acinar cells was maintained after the photodynamic action of SALPC. It is concluded that the stimulation of amylase secretion and membrane permeabilization by SALPC is due to the generation of singlet oxygen. However, the consistent difference between the time course of amylase secretion and membrane permeabilization makes it likely that an initial stage in photodynamic drug action involves oxidation of plasma membrane protein and activation of secretagogue receptors or the G-proteins and their effector systems.

Amylases↗
PubMed1990

Photodynamic action of sulphonated aluminium phthalocyanine (SALPC) on AR4-2J cells, a carcinoma cell line of rat exocrine pancreas.

The photodynamic effects of sulphonated aluminium phthalocyanine (SALPC) have been compared on cultured AR4-2J cells of a pancreatic carcinoma cell line and on exocrine cells of the normal phenotype freshly isolated from the rat pancreas; a multi-channel perifusion system was used for this kinetic study in vitro. Whereas light alone or SALPC alone was without effect on either cell type, photon activation of cellularly-bound SALPC with light greater than 570 nm permeabilised the cells and caused an increase in amylase secretion from normal acinar cells but a dose-dependent inhibition (10(-7) to 10(-5) M) of amylase release from AR4-2J cells. In contrast, direct permeabilisation of the plasma membrane with digitonin, 10 micrograms ml-1, evoked a marked release of amylase from both types of cell. Elevation of [Ca2+]i by the ionophore A23187, 10(-6) M, elicited secretion of amylase from normal cells but had little effect on AR4-2J cells. Finally, it was established that the differential photodynamic effects of SALPC on amylase release were not attributable to any topographical differences in the microanatomical organisation of normal or tumour-derived cells; furthermore, the structural integrity of normal and AR4-2J cells was maintained after the photodynamic action of SALPC. It is concluded that the generation of singlet oxygen is responsible for permeabilisation of both types of cell and that photon-activated SALPC has functionally distinct effects on the constitutive secretion of amylase of tumour cells and the regulated secretory pathway of normal cells. These observations may be important in the development of drugs with a selective photodynamic action on pancreatic tumour cells.

Amylases↗
PubMed1989

Photodynamic action of rose bengal on isolated rat pancreatic acini: stimulation of amylase release.

The halogenated fluorescein derivative, rose bengal, upon photon activation, elicits amylase secretion from isolated, perifused pancreatic acini. This effect is due to production of highly reactive singlet delta oxygen which can permeabilize the cell membrane and may also react chemically with secretagogue receptors, or other functional components of the membrane such as the G-proteins. The profile of photodynamically induced amylase secretion is anion-dependent: it becomes biphasic when the chloride ion is substituted by the glutamate ion, an effect attributed to the action of glutamate on the ionic transport systems of the zymogen granule membrane.

Amylases↗