scholarly journals Inositol phosphates in the duckweed Spirodela polyrhiza L

1996 ◽  
Vol 314 (1) ◽  
pp. 215-225 ◽  
Author(s):  
Charles A. BREARLEY ◽  
David E. HANKE
Keyword(s):  
Developmental Stage ◽  
Higher Plants ◽  
Inositol Phosphates ◽  
Second Messengers ◽  
Direct Link ◽  
Spirodela Polyrhiza ◽  
Massive Accumulation

We have undertaken an analysis of the inositol phosphates of Spirodela polyrhiza at a developmental stage when massive accumulation of InsP6 indicates that a large net synthesis is occurring. We have identified Ins3P, Ins(1,4)P2, Ins(3,4)P2 and possibly Ins(4,6)P2, Ins(3,4,6)P3, Ins(3,4,5,6)P4, Ins(1,3,4,5,6)P5, D- and/or L-Ins(1,2,4,5,6)P5 and InsP6 and revealed the likely presence of a second InsP3 with chromatographic properties similar to Ins(1,4,5)P3. The higher inositol phosphates identified show no obvious direct link to pathways of metabolism of second messengers purported to operate in higher plants, nor do they resemble the immediate products of plant phytase action on InsP6.

scholarly journals Rapid accumulation of inositol trisphosphate reveals that agonists hydrolyse polyphosphoinositides instead of phosphatidylinositol

1983 ◽  
Vol 212 (3) ◽  
pp. 849-858 ◽  
Author(s):  
M J Berridge
Keyword(s):  
Inositol Phosphates ◽  
Second Messengers ◽  
Inositol Phospholipids ◽  
Hormone Sensitive ◽  
High Level ◽  
Phosphatidylinositol 4 ◽  
Energy Dependent ◽  
Hydrolysis Of ◽  
Massive Accumulation ◽  
Primary Action

The agonist-dependent hydrolysis of inositol phospholipids was investigated by studying the breakdown of prelabelled lipid or by measuring the accumulation of inositol phosphates. Stimulation of insect salivary glands with 5-hydroxytryptamine for 6 min provoked a rapid disappearance of [3H]phosphatidylinositol 4,5-bisphosphate [PtdIns(4,5)P2] and [3H]phosphatidylinositol 4-phosphate (PtdIns4P) but had no effect on the level of [3H]phosphatidylinositol (PtdIns). The breakdown of PtdIns(4,5)P2 was associated with a very rapid release of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], which reached a peak 5 1/2 times that of the resting level after 5 s of stimulation. This high level was not maintained but declined to a lower level, perhaps reflecting the disappearance of PtdIns(4,5)P2. 5-Hydroxytryptamine also induced a rapid and massive accumulation of inositol 1,4-bisphosphate [Ins(1,4)P2]. The fact that these increases in Ins(1,4,5)P3 and Ins(1,4)P2 precede in time any increase in the level of inositol 1-phosphate or inositol provides a clear indication that the primary action of 5-hydroxytryptamine is to stimulate the hydrolysis of PtdIns(4,5)P2 to yield diacylglycerol and Ins(1,4,5)P3. The latter is then hydrolysed by a series of phosphomonoesterases to produce Ins(1,4)P2, Ins1P and finally inositol. The very rapid agonist-dependent increases in Ins(1,4,5)P3 and Ins(1,4)P2 suggests that they could function as second messengers, perhaps to control the release of calcium from internal pools. The PtdIns(4,5)P2 that is used by the receptor mechanism represents a small hormone-sensitive pool that must be constantly replenished by phosphorylation of PtdIns. Small changes in the size of this small energy-dependent pool of polyphosphoinositide will alter the effectiveness of the receptor mechanism and could account for phenomena such as desensitization and super-sensitivity.

scholarly journals Inositol phosphate metabolism in bradykinin-stimulated human A431 carcinoma cells. Relationship to calcium signalling

1987 ◽  
Vol 244 (1) ◽  
pp. 129-135 ◽  
Author(s):  
B C Tilly ◽  
P A van Paridon ◽  
I Verlaan ◽  
K W A Wirtz ◽  
S W de Laat ◽  
...  
Keyword(s):  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Second Messengers ◽  
Calcium Signalling ◽  
Carcinoma Cells ◽  
A431 Cells ◽  
Inositol Phosphate Metabolism ◽  
Transient Rise ◽  
Lag Period ◽  
Massive Accumulation

Stimulation of human A431 epidermoid carcinoma cells by bradykinin causes a very rapid release of inositol phosphates and a transient rise in cytoplasmic free Ca2+ concentration ([Ca2+]i). Bradykinin-induced inositol phosphate formation is half-maximal at a concentration of 4 nM and is not affected by pertussis toxin. H.p.l.c. analysis of the various inositol phosphates shows an immediate but transient accumulation of inositol 1,4,5-trisphosphate [Ins(1,4,5)P3], which reaches a peak value of approx. 10 times the basal level within 15 s and slightly precedes the rise in [Ca2+]i, both parameters changing in parallel. After a lag period, bradykinin also induces a massive accumulation of Ins(1,3,4)P3 and inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. Our data support the view that part of the newly formed Ins(1,4,5)P3 is converted into Ins(1,3,4)P3 phosphorylation/dephosphorylation with Ins(1,3,4,5)P4 as intermediate. Furthermore, A431 cells were found to contain strikingly high basal levels of two other inositol phosphates, presumably inositol pentakisphosphate (InsP5) and inositol hexakisphosphate (InsP6), representing more than 50% of the total 3H radioactivity incorporated into inositol phosphates. The presumptive InsP5 and InsP6 are only slightly affected by bradykinin. Although Ins(1,3,4)P3 and InsP4 could function as second messengers, our results suggest that, unlike Ins(1,4,5)P3, neither Ins(1,3,4)P3 nor InsP4 are involved in Ca2+ mobilization.

scholarly journals Metabolic evidence for the order of addition of individual phosphate esters in the myo-inositol moiety of inositol hexakisphosphate in the duckweed Spirodela polyrhiza L

1996 ◽  
Vol 314 (1) ◽  
pp. 227-233 ◽  
Author(s):  
Charles A. BREARLEY ◽  
David E. HANKE
Keyword(s):  
Inositol Phosphates ◽  
Preceding Paper ◽  
Phosphate Esters ◽  
Equilibrium Conditions ◽  
Comprehensive Description ◽  
Monocotyledonous Plant ◽  
Spirodela Polyrhiza ◽  
Synthetic Sequence ◽  
Massive Accumulation ◽  
Inositol Ring

The aquatic monocotyledonous plant Spirodela polyrhiza was labelled with [32P]Pi for short periods under non-equilibrium conditions. An InsP6 fraction was obtained and dissected by using enantiospecific (enzymic) and non-enantiospecific (chemical) means to determine the relative labelling of individual phosphate substituents on the inositol ring of InsP6. Phosphates in positions D-1, -2, -3, -4, -5 and -6 contained approx. 21%, 32–39%, 9–10%, 14–16%, 19–23% and 16–18% of the label respectively. We conclude from the foregoing, together with identities [described in the preceding paper, Brearley and Hanke (1996) Biochem. J. 314, 215–225] of inositol phosphates found in this plant at a developmental stage associated with massive accumulation of InsP6, that synthesis of InsP6 from myo-inositol proceeds according to the sequence Ins3P → Ins(3,4)P2 → Ins(3,4,6)P3 → Ins(3,4,5,6)P4 → Ins(1,3,4,5,6)P5 → Ins P6 in Spirodela polyrhiza. These results represent the first description of the synthetic sequence to InsP6 in the plant kingdom and the only comprehensive description of endogenous inositol phosphates in any plant tissue. The sequence described differs from that reported in the slime mould Dictyostelium discoideum.

scholarly journals Natural polyamines stimulate G-proteins

1992 ◽  
Vol 282 (2) ◽  
pp. 545-550 ◽  
Author(s):  
J L Bueb ◽  
A Da Silva ◽  
M Mousli ◽  
Y Landry
Keyword(s):  
Mast Cells ◽  
Pertussis Toxin ◽  
Inositol Phosphates ◽  
Second Messengers ◽  
G Protein Coupled Receptors ◽  
Extracellular Signals ◽  
Physiological Relevance ◽  
G Protein Coupled ◽  
Stimulation Of ◽  
Rat Mast Cells

The natural polyamines spermine and spermidine, the biosynthetic precursor putrescine and their analogues cadaverine and tyramine stimulate the GTPase activity of purified GTP-binding proteins (Go/Gi) from calf brain reconstituted into phospholipid vesicles. The order of potency was spermine greater than spermidine greater than putrescine = cadaverine greater than tyramine. The physiological relevance of this observation was assessed, showing the same order of potency of polyamines in the stimulation of peritoneal and tracheal rat mast cells. The activation of rat mast cells by polyamines was inhibited by benzalkonium chloride or by a 2 h pretreatment of the cells with pertussis toxin. The increase in inositol phosphates evoked by polyamines was also inhibited by pertussis toxin. Therefore we propose that intracellular polyamines might control the basal level of second messengers and modulate extracellular signals transduced through G-protein-coupled receptors.

Adrenergic stimulation of inositol phosphate accumulation in tracheal epithelium

1989 ◽  
Vol 66 (1) ◽  
pp. 504-508 ◽  
Author(s):  
T. Bainbridge ◽  
R. D. Feldman ◽  
M. J. Welsh
Keyword(s):  
Adrenergic Receptor ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Second Messengers ◽  
Receptor Activation ◽  
Adrenergic Stimulation ◽  
Cl Secretion ◽  
Phosphate Accumulation ◽  
Inositol Phosphate Accumulation ◽  
Stimulation Of

To determine whether inositol phosphates are important second messengers in the regulation of Cl- secretion by airway epithelia, we examined the relationship between inositol phosphate accumulation and Cl- secretion in response to adrenergic agonists. We found that epinephrine stimulated Cl- secretion and inositol phosphate accumulation with similar concentration dependence. Although isoproterenol stimulated Cl- secretion, there was no effect of beta-adrenergic receptor activation on inositol phosphate accumulation. In contrast, alpha 1-adrenergic receptor activation stimulated inositol phosphate accumulation but failed to induce Cl- secretion. Another Cl- secretagogue, prostaglandin E1, also failed to stimulate inositol phosphate accumulation. These data suggest that inositol phosphate accumulation is neither sufficient nor required for stimulation of Cl- secretion in cultured canine tracheal epithelial cells.

Contractile responses and signal transduction of endothelin-1 in aorta and mesenteric vasculature of adult spontaneously hypertensive rats

1993 ◽  
Vol 71 (7) ◽  
pp. 473-483 ◽  
Author(s):  
Paul V. Nguyen ◽  
Xiao-Ping Yang ◽  
Guo Li ◽  
Li Yuan Deng ◽  
Jean-Pierre Flückiger ◽  
...  
Keyword(s):  
Inositol Phosphates ◽  
Second Messengers ◽  
Resistance Arteries ◽  
Hypertensive Rats ◽  
Contractile Responses ◽  
Spontaneously Hypertensive ◽  
Wky Rats ◽  
Mesenteric Arterial Bed ◽  
Mesenteric Vessels ◽  
Wistar Kyoto

The contractile responses and generation of intracellular second messengers in response to endothelin-1 (ET-1), a potent vasoconstrictor peptide released locally by endothelial cells and involved in the regulation of vascular tone, were investigated in different segments of the vascular tree of adult 18-week-old spontaneously hypertensive rats (SHR) as compared with age-matched Wistar–Kyoto (WKY) rats. Aorta rings of SHR showed lower maximum response to ET-1 in comparison with WKY rats. Rings of the main superior mesenteric artery of SHR and WKY showed similar responses to ET-1. Small mesenteric resistance arteries of SHR, mounted on a wire myograph, developed similar tension to those of WKY rats in response to ET-1. The dose–response of inositol phosphates to ET-1 was significantly blunted in thoracic aorta of SHR compared with WKY rats, whereas it was similar in the mesenteric arterial bed. Baseline 1,2-diacylglycerol content was higher in thoracic aorta of SHR than WKY, while it was similar in the mesenteric arterial bed of the two strains. The response of 1,2-diacylglycerol to ET-1 was blunted in aorta of SHR, whereas no significant differences in diacylglycerol accumulation could be found in mesenteric vessels between SHR and WKY. In small mesenteric arteries, the dose–response to ET-1 of cytosolic free calcium, measured with the fluorescent dye Fura 2-AM, was similar in the two groups of rats. We conclude that in the aorta of 18-week-old SHR there is reduced generation of second messengers (inositol phosphates and diacylglycerol), which underlies its decreased response to ET-1 In mesenteric vessels (both proximal and distal) signal transduction is similar in SHR and WKY, and as a result contractile responses in both species are comparable. The responses to ET-1 of the arterial tree in terms of contractility and second messenger generation may reflect the adaptive processes taking place as a consequence of elevated blood pressure within the arterial wall of different segments of the vasculature of SHR.Key words: inositol phosphate, phospholipids, diacylglycerol, cytosolic calcium, second messengers, conduit and resistance arteries, Wistar–Kyoto rats.

scholarly journals Capacitative calcium entry in parotid acinar cells

1989 ◽  
Vol 258 (2) ◽  
pp. 409-412 ◽  
Author(s):  
H Takemura ◽  
J W Putney
Keyword(s):  
Plasma Membrane ◽  
Inositol Phosphates ◽  
Second Messengers ◽  
Acinar Cells ◽  
Receptor Activation ◽  
Initial Increase ◽  
Muscarinic Agonist ◽  
Plasma Membrane Permeability ◽  
Parotid Acinar Cells ◽  
Parotid Cells

The intracellular Ca2+ indicator, fura-2, was used to monitor changes in cytosolic [Ca2+] in parotid acinar cells. When parotid cells were incubated in a medium containing low [Ca2+], and [Ca2+] was restored to the physiological range, there was a small increase in cytosolic [Ca2+]. If, however, the cells were first activated by a muscarinic agonist, and receptor activation was terminated before the addition of Ca2+ by the addition of a pharmacological excess of the muscarinic-receptor antagonist atropine, the initial increase in cytosolic [Ca2+] was faster and transiently larger than in the control cells which had not been previously stimulated. This suggested that a stimulation of Ca2+ entry occurred owing to the prior emptying of the agonist-regulated intracellular Ca2+ pool. This extra Ca2+ influx seen in pool-depleted cells persisted even when the interval between the addition of atropine and Ca2+ was increased from 1 to 20 min. Also, when the pool was allowed to refill by adding atropine in the presence of extracellular Ca2+, and Ca2+ was then sequentially removed and restored, the rise in cytosolic [Ca2+] after the addition of extracellular Ca2+ was not rapid, and resembled the increase seen in unstimulated cells. These results indicate that, when the agonist-sensitive Ca2+ pool is emptied by an agonist, Ca2+ influx across the plasma membrane is increased. This influx of Ca2+ occurs independently of the concentrations of inositol phosphates and probably of any second messengers linked directly to receptor activation. It appears rather to be a consequence of the empty state of the Ca2+ pool. Further, we suggest that, whenever the agonist-sensitive Ca2+ pool is emptied by agonist activation, the plasma-membrane permeability to Ca2+ will be increased, and this may account, at least in part, for the phenomenon of receptor-activated Ca2+ entry.

Involvement of second messengers and protein phosphorylation in astrocyte swelling

1992 ◽  
Vol 70 (S1) ◽  
pp. S362-S366 ◽  
Author(s):  
A. S. Bender ◽  
J. T. Neary ◽  
M. D. Norenberg
Keyword(s):  
Cyclic Amp ◽  
Protein Phosphorylation ◽  
Volume Regulation ◽  
Inositol Phosphates ◽  
Inositol Phosphate ◽  
Second Messengers ◽  
Astrocyte Swelling ◽  
Regulatory Processes ◽  
Intracellular Signals ◽  
Dependent Protein

In a hypoosmotic model of astrocyte swelling, we found that Ca2+ and intracellular signals such as diacylglycerol and inositol phosphate, as well as protein phosphorylation systems, are implicated in the generation and (or) modulation of volume regulatory processes. Cyclic AMP, which also has a significant effect on astrocyte volume regulation, in addition influences some of these second messengers.Key words: astrocyte, Ca2+-dependent protein kinases, Ca2+ influx, cell volume, cyclic AMP, inositol phosphates, protein phosphorylation.

scholarly journals Histamine inhibits adrenocortical cell proliferation but does not affect steroidogenesis

2014 ◽  
Vol 221 (1) ◽  
pp. 15-28 ◽  
Author(s):  
Romina Maria Pagotto ◽  
Elba Nora Pereyra ◽  
Casandra Monzón ◽  
Carolina Mondillo ◽  
Omar Pedro Pignataro
Keyword(s):  
Histidine Decarboxylase ◽  
Inositol Phosphates ◽  
Second Messengers ◽  
Experimental Models ◽  
Adrenocortical Cell ◽  
Adrenocortical Cells ◽  
Tumor Pathology ◽  
Cycle Arrest ◽  
M Phase ◽  
H295r Cells

Histamine (HA) is a neurotransmitter synthesized in most mammalian tissues exclusively by histidine decarboxylase enzyme. Among the plethora of actions mediated by HA, the modulatory effects on steroidogenesis and proliferation in Leydig cells (LCs) have been described recently. To determine whether the effects on LCs reported could be extrapolated to all steroidogenic systems, in this study, we assessed the effect of this amine on adrenal proliferation and steroidogenesis, using two adrenocortical cell lines as experimental models, murine Y1 cells and human NCI-H295R cells. Even when steroidogenesis was not modified by HA in adrenocortical cells, the biogenic amine inhibited the proliferation of H295R cells. This action was mediated by the activation of HRH1 subtype and an increase in the production of inositol phosphates as second messengers, causing cell-cycle arrest in the G2/M phase. These results indicate a new role for HA in the proliferation of human adrenocortical cells that could contribute to a better understanding of tumor pathology as well as to the development of new therapeutic agents.

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