scholarly journals Zn disrupts Cd‐induced stimulation of apical choline uptake in cultured choroid plexus independent of GSH availability (685.4)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
A. Villalobos ◽  
R Young ◽  
S Francis Stuart
Keyword(s):  
Choroid Plexus ◽  
Choline Uptake ◽  
Stimulation Of

scholarly journals GSH and Zinx Supplementation Attenuate Cadmium-Induced Cellular Stress and Stimulation of Choline Uptake in Cultured Neonatal Rat Choroid Plexus Epithelia

2021 ◽  
Vol 22 (16) ◽  
pp. 8857
Author(s):  
Samantha D. Francis Stuart ◽  
Alice R. Villalobos
Keyword(s):  
Choroid Plexus ◽  
Cellular Stress ◽  
Stress Protein ◽  
Buthionine Sulfoximine ◽  
Neonatal Rat ◽  
Choline Uptake ◽  
Glutamate Cysteine Ligase ◽  
Rate Limiting ◽  
Stimulation Of

Choroid plexus (CP) sequesters cadmium and other metals, protecting the brain from these neurotoxins. These metals can induce cellular stress and modulate homeostatic functions of CP, such as solute transport. We previously showed in primary cultured neonatal rat CP epithelial cells (CPECs) that cadmium induced cellular stress and stimulated choline uptake at the apical membrane, which interfaces with cerebrospinal fluid in situ. Here, in CPECs, we characterized the roles of glutathione (GSH) and Zinx supplementation in the adaptive stress response to cadmium. Cadmium increased GSH and decreased the reduced GSH-to-oxidized GSH (GSSG) ratio. Heat shock protein-70 (Hsp70), heme oxygenase (HO-1), and metallothionein (Mt-1) were induced along with the catalytic and modifier subunits of glutamate cysteine ligase (GCL), the rate-limiting enzyme in GSH synthesis. Inhibition of GCL by l-buthionine sulfoximine (BSO) enhanced stress protein induction and stimulation of choline uptake by cadmium. Zinx alone did not induce Hsp70, HO-1, or GCL subunits, or modulate choline uptake. Zinx supplementation during cadmium exposure attenuated stress protein induction and stimulation of choline uptake; this effect persisted despite inhibition of GSH synthesis. These data indicated up-regulation of GSH synthesis promotes adaptation to cadmium-induced cellular stress in CP, but Zinx may confer cytoprotection independent of GSH.

scholarly journals Stress-induced stimulation of choline transport in cultured choroid plexus epithelium exposed to low concentrations of cadmium

2014 ◽  
Vol 306 (5) ◽  
pp. R291-R303 ◽  
Author(s):  
Robin K. Young ◽  
Alice R. A. Villalobos
Keyword(s):  
Heavy Metals ◽  
Map Kinase ◽  
Choroid Plexus ◽  
Stress Proteins ◽  
Neonatal Rat ◽  
Choline Uptake ◽  
Choroid Plexus Epithelium ◽  
Choline Transport ◽  
Low Concentrations ◽  
Stimulation Of

The choroid plexus epithelium forms the blood-cerebrospinal fluid barrier and accumulates essential minerals and heavy metals. Choroid plexus is cited as being a “sink” for heavy metals and excess minerals, serving to minimize accumulation of these potentially toxic agents in the brain. An understanding of how low doses of contaminant metals might alter transport of other solutes in the choroid plexus is limited. Using primary cultures of epithelial cells isolated from neonatal rat choroid plexus, our objective was to characterize modulation of apical uptake of the model organic cation choline elicited by low concentrations of the contaminant metal cadmium (CdCl2). At 50–1,000 nM, cadmium did not directly decrease or increase 30-min apical uptake of 10 μM [3H]choline. However, extended exposure to 250–500 nM cadmium increased [3H]choline uptake by as much as 75% without marked cytotoxicity. In addition, cadmium induced heat shock protein 70 and heme oxygenase-1 protein expression and markedly induced metallothionein gene expression. The antioxidant N-acetylcysteine attenuated stimulation of choline uptake and induction of stress proteins. Conversely, an inhibitor of glutathione synthesis l-buthionine-sulfoximine (BSO) enhanced stimulation of choline uptake and induction of stress proteins. Cadmium also activated ERK1/2 MAP kinase. The MEK1 inhibitor PD98059 diminished ERK1/2 activation and attenuated stimulation of choline uptake. Furthermore, inhibition of ERK1/2 activation abated stimulation of choline uptake in cells exposed to cadmium with BSO. These data indicate that in the choroid plexus, exposure to low concentrations of cadmium may induce oxidative stress and consequently stimulate apical choline transport through activation of ERK1/2 MAP kinase.

Stimulation of area postrema decreases blood flow to choroid plexus

1991 ◽  
Vol 260 (3) ◽  
pp. H902-H908 ◽  
Author(s):  
J. L. Williams ◽  
M. M. Thebert ◽  
K. A. Schalk ◽  
D. D. Heistad
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Choroid Plexus ◽  
Area Postrema ◽  
Blood Gases ◽  
Autonomic Ganglia ◽  
Lateral Ventricles ◽  
Anesthetized Dogs ◽  
The Central Nervous System ◽  
Stimulation Of

The goal of this study was to examine effects of stimulation of the area postrema on blood flow to choroid plexus and brain. In chloralose-anesthetized dogs, the area postrema was stimulated electrically, and arterial pressure and blood gases were maintained at control levels. We measured blood flow to brain and choroid plexus of the fourth and lateral ventricles with microspheres. Stimulation of the area postrema at 10 +/- 2 microA (means +/- SE), which was the threshold for changes in arterial pressure and heart rate, decreased blood flow to choroid plexus of the fourth and lateral ventricles by 41 +/- 11 and 51 +/- 6%, respectively (from 349 +/- 38 and 503 +/- 46 ml.min-1.100 g-1, respectively). Stimulation at high amplitudes (67 +/- 5 microA) produced only slightly greater decreases in blood flow to choroid plexus. In contrast, cerebral blood flow did not change during stimulation of the area postrema. After blockade of autonomic ganglia with intravenous chlorisondamine, stimulation of the area postrema had minimal effects on blood flow to choroid plexus. The results indicate that stimulation of the area postrema decreases blood flow to choroid plexus, probably by an autonomic mechanism. We speculate that the area postrema may play a role in regulation of volume in the central nervous system by modulating production of cerebrospinal fluid.

5-HT1C receptor-mediated stimulation of inositol phosphate production in pig choroid plexus

1989 ◽  
Vol 339 (3) ◽  
Author(s):  
Daniel Hoyer ◽  
Christian Waeber ◽  
Philippe Schoeffter ◽  
JoseMaria Palacios ◽  
Anant Dravid
Keyword(s):  
Choroid Plexus ◽  
Inositol Phosphate ◽  
Inositol Phosphate Production ◽  
Stimulation Of

scholarly journals Antagonism of phorbol-ester-stimulated phosphatidylcholine biosynthesis by the phospholipid analogue hexadecylphosphocholine

1993 ◽  
Vol 291 (2) ◽  
pp. 561-567 ◽  
Author(s):  
T Wieder ◽  
C C Geilen ◽  
W Reutter
Keyword(s):  
Cell Lines ◽  
Hela Cells ◽  
Mdck Cells ◽  
Fold Increase ◽  
Choline Uptake ◽  
Choline Incorporation ◽  
Contrast Enhanced ◽  
Phosphatidylcholine Biosynthesis ◽  
Membrane Bound ◽  
Stimulation Of

The antagonization of phorbol 12-myristate 13-acetate (PMA)-stimulated phosphatidylcholine (PtdCho) biosynthesis by the phospholipid analogue hexadecylphosphocholine (HePC) in MDCK cells was investigated and compared with the corresponding influence in HeLa cells. In both cell lines, PMA-stimulated PtdCho biosynthesis was antagonized by 50 microM HePC. However, subsequent experiments provided evidence that PMA enhances PtdCho biosynthesis by at least two mechanisms: (i) by stimulation of choline uptake and (ii) by translocation of CTP:choline phosphate cytidylyltransferase to membranes. In MDCK cells, 5 nM PMA caused a 4-fold increase in [methyl-3H]choline incorporation into PtdCho, which was paralleled by an approx. 2-fold stimulation of choline uptake. These data indicate that choline uptake might play an important role in the regulation of PtdCho biosynthesis in this cell line, especially since we could not detect any significant increase in membrane-bound cytidyltransferase activity in PMA-treated MDCK cells. In contrast, enhanced PtdCho biosynthesis in HeLa cells is achieved by a 2-fold increase in particulate cytidylyltransferase activity after PMA stimulation. Translocation of cytidylyltransferase from the cytosol to membranes is therefore important in HeLa cells. Nevertheless, in both cell lines, the main target of HePC seems to be the translocation process. In MDCK cells, addition of 50 microM HePC decreases membrane-bound cytidylyltransferase activity by about 45%, compared with control cells and PMA-treated cells. In HeLa cells, PMA-induced translocation of cytidylyltransferase to membranes is totally abolished by HePC.

Stimulation of renal phospholipid formation during potassium depletion.

1977 ◽  
Vol 233 (3) ◽  
pp. E212
Author(s):  
F G Toback ◽  
L J Havener ◽  
B H Spargo
Keyword(s):  
Potassium Depletion ◽  
Choline Uptake ◽  
Renal Cells ◽  
Renal Growth ◽  
Kennedy Pathway ◽  
Choline Incorporation ◽  
And Control ◽  
Choline Phosphoglyceride ◽  
Cortical Slices ◽  
Stimulation Of

Potassium depletion induces increased membrane phospholipid formation and renal growth in rats. To determine the mechanism by which potassium depletion augments phospholipid formation, the metabolism of radioactive choline, a precursor of choline-containing phospholipids, was studied in renal slices. Cortical and medullary tissue from potassium-depleted and control animals accumulated extracellular choline and sequentially converted it to phosphorylcholine, cytidine diphosphocholine (CDP-choline), and choline phosphoglyceride, thereby demonstrating that renal cells can utilize the Kennedy pathway for phospholipid synthesis. [14C]Choline uptake into intracellular fluid was increased in cortical slices from potassium-depleted animals. The apparent Km and Vmax of the kinase reaction which converts entering [14C]choline to [14C]phosphorylcholine were unchanged during potassium depletion. The rate of [14C]phosphorylcholine conversion to [14C]CDP-choline was also unchanged. In contrast, the Vmax of [14C]choline phosphoglyceride formation from [14C]CDP-choline was increased, whereas the apparent Km for this reaction was unchanged. These results indicate that increased renal choline phosphoglyceride formation during potassium depletion can occur via the Kennedy pathway and appears to be mediated by increases in choline uptake and the rate of CDP-choline incorporation into phospholipid, the first and last steps of the pathway.

scholarly journals PHYSIOLOGICAL STIMULATION OF THE CHOROID PLEXUS AND EXPERIMENTAL POLIOMYELITIS

1918 ◽  
Vol 27 (6) ◽  
pp. 679-687 ◽  
Author(s):  
Simon Flexner ◽  
Harold L. Amoss ◽  
Frederick Eberson
Keyword(s):  
Cerebrospinal Fluid ◽  
Choroid Plexus ◽  
Intravenous Injection ◽  
Structural Changes ◽  
Intravenous Injections ◽  
Resistance To Infection ◽  
The Individual ◽  
Intravenous Inoculation ◽  
Stimulation Of

The experiments recorded in this paper serve, in the first place, to confirm the experiments of Dixon and Halliburton on the stimulating effect of intravenous injections of extracts of choroid plexus in the secretion of the cerebrospinal fluid, and extend their observations to monkeys. They bring out also the variable effects of the virus of poliomyelitis, variations affected by the quality of the virus and also by the individual powers of resistance to infection possessed by individual monkeys. These factors of variation must be taken into account in performing and interpreting experiments on infection and particularly those on immunity and specific therapy in relation to poliomyelitis. In general it may be said that experimental infection by way of the blood is not easy to produce in monkeys unless some contributing factor, such as the existence of a coincident aseptic meningitis, operates at the same time. And yet Experiments 1 and 2 show that when the strength of the virus is great the injection of relatively considerable quantities suffices to induce infection and paralysis, but not in all instances. The chief outcome of the experiments has been to determine the fact that when the intravenous inoculation of the virus does not in itself suffice to induce infection and paralysis, the intravenous injection of extracts of the choroid plexus, which in themselves excite the secretory functions which preside over the formation of the cerebrospinal fluid, is powerless to modify this result. This fact would seem to be of interest and importance, since it has already been shown that very slight structural changes in the meningeal-choroidal complex suffice to make possible or certain infection under these circumstances. Apparently mere augmentation, from time to time, of the secretory functions of the choroid plexus, through intravenous injection of an extract of the choroid plexus and while the virus is still circulating, is insufficient to insure passage of the virus from the blood into the nervous tissues, upon which infection depends. Neither does the augmentation exercise a restraining influence on the development of infection otherwise capable of taking place.

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