Role of extracellular calcium in in vitro uptake and intraphagocytic location of macrolides

In vitro uptake of 67Ga-citrate and 59Fe-citrate by DS sarcoma cells in the presence of tumor-bearing animal blood plasma showed a dramatic inhibition of both 67Ga and 59Fe uptakes: about ii/io of 67Ga and 1/5o of the 59Fe are taken up by the cells. Subcellular fractionation appears to indicate no specific binding to cell structures, and the difference of binding seems to be related to the transferrin chelation and transmembrane transport differences

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Human placental lactogen release in vitro: paradoxical effects of calcium

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1981.240.5.e550 ◽

1981 ◽

Vol 240 (5) ◽

pp. E550-E555

Author(s):

S. Handwerger ◽

P. M. Conn ◽

J. Barrett ◽

S. Barry ◽

A. Golander

Keyword(s):

Calcium Influx ◽

Extracellular Calcium ◽

Calcium Flux ◽

Placental Lactogen ◽

Human Placental Lactogen ◽

Paradoxical Effects ◽

Subsequent Exposure ◽

Normal Calcium

To study the effects of calcium on the release of human placental lactogen (hPL), placental explants were exposed to media containing lower or higher concentrations of calcium than normally available to the placenta. Explants exposed for 2 h to calcium-poor medium or medium containing either 2 mM EDTA or 2 mM EGTA released 160, 248, and 253% more hPL, respectively, than control explants. In contrast, explants exposed to medium containing higher than normal calcium concentrations released the same amounts of hPL as the control explants. At lower than normal extracellular calcium concentrations, the increased hPL release was inversely proportional to the calcium concentration. The increased release in calcium-poor medium was inhibited by subsequent exposure of the explants to medium containing calcium and was prevented by either barium or magnesium. Changes in barium or magnesium concentrations, however, had no effects on hPL release in the presence of normal extracellular calcium concentrations. Methoxyverapamil (D 600), an inhibitor of calcium flux, stimulated hPL release. Because low extracellular calcium and methoxyverapamil both inhibit calcium influx, these experiments suggest that calcium influx inhibits hPL release. The role of calcium in the regulation of hPL release therefore appears to be different from that reported in other release systems.

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In vitro uptake of vitellogenin by follicles of the cockroach Nauphoeta cinerea: Comparison of artificial media with haemolymph media and role of vitellogenin concentration and of juvenile hormone

Journal of Insect Physiology ◽

10.1016/0022-1910(88)90196-5 ◽

1988 ◽

Vol 34 (6) ◽

pp. 541-548 ◽

Cited By ~ 19

Author(s):

Helmut Kindle ◽

Rolf König ◽

Beatrice Lanzrein

Keyword(s):

Juvenile Hormone ◽

Nauphoeta Cinerea ◽

In Vitro Uptake ◽

Vitellogenin Concentration

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Role of LDL receptors in the in vitro uptake and degradation of LDL in the media of rabbit thoracic aorta.

Circulation Research ◽

10.1161/01.res.64.5.957 ◽

1989 ◽

Vol 64 (5) ◽

pp. 957-967 ◽

Cited By ~ 2

Author(s):

P A Curmi ◽

G Renaud ◽

L Juan ◽

B Chiron ◽

A Tedgui

Keyword(s):

Thoracic Aorta ◽

Ldl Receptors ◽

The Media ◽

In Vitro Uptake

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The role of a metal-transferrin-transferrin-receptor mechanism if the in vitro uptake of metals by human lymphoblasts (WIL-2)

Inorganica Chimica Acta ◽

10.1016/s0020-1693(00)95260-5 ◽

1983 ◽

Vol 79 ◽

pp. 223-224 ◽

Cited By ~ 1

Author(s):

J. Duffield ◽

F. Planas-Bohne ◽

D.M. Taylor

Keyword(s):

Transferrin Receptor ◽

In Vitro Uptake

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Procalcific effect of proprotein convertase subtilisin/kexin type 9 (PCSK9) in chronic kidney disease (CKD)

European Heart Journal ◽

10.1093/ehjci/ehaa946.3652 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

N Ferri ◽

M.G.P Lupo ◽

M.R Rattazzi

Keyword(s):

Colorimetric Assay ◽

Extracellular Calcium ◽

Calcium Deposition ◽

Standard Diet ◽

Plasma Total Cholesterol ◽

Calcium Crystals ◽

Positive Effect

Abstract Aim PCSK9 has been recently associated with a higher rate of calcification in hypercholesterolemic, diabetes and CKD patients. The aim of this study was thus to investigate the role of PCSK9 in VC process, under uremic condition, both on in vivo and in vitro experimental settings. Methods Sprauge Dawley rats were fed a standard diet (SD, n=11) or uremic diet (UD, n=11) for 6 weeks. Calcium crystals in aortas were visualized by von Kossa staining and quantified by a colorimetric assay and plasma total cholesterol determined. Control and PCSK9-overexpressing smooth muscle cells (SMCsPCSK9) were cultured with 2.5% FCS ± Pi for 7 days. Hydroxyapatite deposition by SMCs was measured by a colorimetric assay. The number and the content of pro-calcific extracellular vesicles (EVs) budding from the cells were determined. Results The hyperphosphatemia secondary to CKD lead to rat aortic calcification (+7.3-fold) and a significant increase in TC and PCSK9 levels (+1.4 and +2.7-fold, respectively). Higher expression of PCSK9 was also observed in kidney (+4.8-fold) and liver (+1.5-fold). SMCsPCSK9 showed higher extracellular calcium deposition (+1.4-fold) in response to Pi and increase EVs production (+7-fold). The incubation of control cells with recombinant PCSK9 did not induce extracellular calcium deposition. Conclusions Our study suggest a positive effect of intracellular PCSK9 on vascular calcification in CKD condition. Pro-calcific budding of EVs seems one of the possible mediators of this process. PCSK9 and calcification Funding Acknowledgement Type of funding source: None

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In Vitro Control of Genes Critical for Parathyroid Embryogenesis by Extracellular Calcium

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa058 ◽

2020 ◽

Vol 4 (7) ◽

Author(s):

Sergio Fabbri ◽

Roberto Zonefrati ◽

Gianna Galli ◽

Giorgio Gronchi ◽

Giuliano Perigli ◽

...

Keyword(s):

Transcription Factors ◽

Mrna Expression ◽

Extracellular Calcium ◽

Variable Response ◽

Messenger Ribonucleic Acid ◽

Low Calcium ◽

Parathyroid Function ◽

High Calcium

Abstract Background The expression of the parathyroid transcription factors, encoded by the genes GATA3, GCM2, and MAFB, persists after parathyroid morphogenesis. This suggests a role of these genes in the regulatory program that governs parathyroid function in the adult. Indeed, these 3 genes form a transcriptional cascade able to activate PTH gene expression. Materials and Methods Adult adenoma parathyroid tissues were put in primary cell culture to evaluate the messenger ribonucleic acid (mRNA) expression of the PTH gene, of the genes involved in the calcium regulatory signaling pathway (CaSR, GNA11, and AP2S1), and of the 3 genes (GATA3, GCM2, and MAFB) involved in the parathyroid morphogenesis in the presence of different extracellular calcium concentrations from 0.1 mM to 3.0 mM. Aim The aim of the study was to investigate whether different extracellular calcium conditions could control the expression of transcription factors critical for parathyroid embryogenesis. Results The results of the experiments showed that the mRNA expression of GATA3, GCM2, and MAFB genes follows the same response as the PTH gene to extracellular calcium concentrations, with the highest expression at low calcium (0.1 mM) and the lowest at high calcium (3.0 mM). Conversely, the genes involved in the calcium signaling in the parathyroid cells showed a variable response to the extracellular calcium concentrations, with the CaSR and GNA11 genes exhibiting a sensitivity to low calcium concentrations. Conclusions These findings indicate that transcription factors recognized for their role in parathyroid embryogenesis show a response to extracellular calcium later in adulthood that parallels the behavior of the PTH gene.

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Role of calcium in the regulation of colonic secretion in the rat

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1983.244.5.g552 ◽

1983 ◽

Vol 244 (5) ◽

pp. G552-G560 ◽

Cited By ~ 1

Author(s):

T. W. Zimmerman ◽

J. W. Dobbins ◽

H. J. Binder

Keyword(s):

Short Circuit ◽

Short Circuit Current ◽

Chloride Secretion ◽

Extracellular Calcium ◽

Electrolyte Transport ◽

Rat Colon ◽

Sodium Absorption ◽

Chloride Absorption

In vitro experiments were performed in rat colon to define the role of calcium in the regulation of electrolyte transport. Neither basal net sodium absorption (JNanet) nor JClnet was affected by varying serosal calcium from 0 to 3.0 mM, but both were decreased by 4.8 mM calcium. Removal of serosal calcium completely inhibited the effect of bethanechol, a muscarinic cholinergic agonist, which inhibits neutral sodium-chloride absorption in 1.2 mM calcium. In contrast, theophylline significantly decreased JNanet and JClnet both in the presence and absence of calcium, but the effects of theophylline were significantly less in calcium-free media. In 3.0 mM calcium bethanechol inhibited JCLnet significantly greater than JNanet and in 4.8 mM calcium bethanechol decreased JClnet equivalent to the increase in short-circuit current without significantly altering JNanet. We conclude that 1) high [Ca2+] inhibits net sodium and net chloride absorption; 2) the alteration of electrolyte transport by bethanechol is dependent on extracellular calcium, and the alteration of electrolyte transport by theophylline is not dependent on extracellular calcium but may be dependent on intracellular calcium; and 3) in addition to inhibition of neutral NaCl absorption, bethanechol stimulates chloride secretion.

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