Calcium entry, mobilization, and extrusion in postcapillary venular endothelium exposed to bradykinin

1993 ◽  
Vol 265 (2) ◽  
pp. H569-H580 ◽  
Author(s):  
M. Ziche ◽  
D. Zawieja ◽  
R. K. Hester ◽  
H. Granger
Keyword(s):  
Endoplasmic Reticulum ◽  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Influx ◽  
Cytosolic Calcium ◽  
Calcium Pump ◽  
Endoplasmic Reticulum Calcium ◽  
Calcium Indicator ◽  
Subsequent Exposure ◽  
Calcium Extrusion

The effect of bradykinin (BK) on cytosolic calcium in coronary venular endothelial cells (CVEC) was studied using the intracellular calcium indicator indo 1. At normal extracellular calcium levels, CVEC responded to BK at concentrations as low as 0.1 pM; maximum cytosolic calcium spikes occurred at 10 nM. In calcium-free medium, poststimulation cytosolic calcium concentration returned to levels below prestimulation values, implying that BK modulates calcium extrusion mechanisms that are normally masked by calcium influx into the cell. To test this hypothesis, we depleted internal stores of calcium using two approaches: preconditioning or blockade of the endoplasmic reticulum calcium pump with the sesquiterpene lactone, thapsigargin. Depletion by preconditioning consisted of two prior doses of BK followed by a third stimulus of the agonist. Under these conditions, the final dose of BK caused a fall, rather than rise, in cytosolic calcium. Thapsigargin blocked the endoplasmic reticulum calcium pump, leading to a steady-state rise in intracellular calcium concentration. Subsequent exposure of these cells to BK also led to a fall in cytosolic calcium. The preconditioning and thapsigargin studies are consistent with a modulation of calcium extrusion processes by BK in CVEC. The signals responsible for this modulation are unknown.

scholarly journals Orientia tsutsugamushi Inhibits Apoptosis of Macrophages by Retarding Intracellular Calcium Release

2002 ◽  
Vol 70 (8) ◽  
pp. 4692-4696 ◽  
Author(s):  
Mee-Kyung Kim ◽  
Seung-Yong Seong ◽  
Ju-Young Seoh ◽  
Tae-Hee Han ◽  
Hyeon-Je Song ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Calcium Release ◽  
Cytosolic Calcium ◽  
Orientia Tsutsugamushi ◽  
Cytosolic Calcium Concentration ◽  
Infected Cells ◽  
Intracellular Calcium Release ◽  
Calcium Redistribution ◽  
In Cells

ABSTRACT Orientia tsutsugamushi shows both pro- and antiapoptotic activities in infected vertebrate cells. Apoptosis of THP-1 cells induced by beauvericin was inhibited by O. tsutsugamushi infection. Beauvericin-induced calcium redistribution was significantly reduced and retarded in cells infected with O. tsutsugamushi. Antiapoptotic activities of O. tsutsugamushi in infected cells are most probably due to inhibition of the increase in the cytosolic calcium concentration.

Presenilin 1 is a direct regulator of the cardiac sarco/endoplasmic reticulum calcium pump

Cell Calcium ◽  
2021 ◽  
pp. 102468
Author(s):  
Elisa Bovo ◽  
Roman Nikolaienko ◽  
Daniel Kahn ◽  
Ellen Cho ◽  
Seth L. Robia ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Pump ◽  
Presenilin 1 ◽  
Endoplasmic Reticulum Calcium ◽  
Direct Regulator

scholarly journals Modulation of endoplasmic reticulum calcium pump expression during lung cancer cell differentiation

FEBS Journal ◽  
2012 ◽  
Vol 280 (21) ◽  
pp. 5408-5418 ◽  
Author(s):  
Atousa Arbabian ◽  
Jean-Philippe Brouland ◽  
Ágota Apáti ◽  
Katalin Pászty ◽  
Luca Hegedűs ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Differentiation ◽  
Cancer Cell ◽  
Calcium Pump ◽  
Lung Cancer Cell ◽  
Endoplasmic Reticulum Calcium

scholarly journals Cytosolic free calcium changes induced by chemotactic peptide in neutrophils from patients with chronic granulomatous disease

Blood ◽  
1984 ◽  
Vol 63 (1) ◽  
pp. 231-233 ◽  
Author(s):  
PD Lew ◽  
C Wollheim ◽  
RA Seger ◽  
T Pozzan
Keyword(s):  
Chronic Granulomatous Disease ◽  
Calcium Concentration ◽  
Cytosolic Calcium ◽  
Human Neutrophils ◽  
Free Calcium ◽  
Granulomatous Disease ◽  
Chemotactic Peptide ◽  
Intact Cells ◽  
Calcium Indicator ◽  
Free Calcium Concentration

Abstract Cytoplasmic free calcium concentration (Ca2+)i was measured in neutrophils from patients with the classical X-linked form of chronic granulomatous disease (CGD) by trapping the fluorescent calcium indicator Quin 2 in intact cells. CGD neutrophils do not produce superoxide and are only slightly depolarized upon stimulation by the chemotactic peptide. N-formyl-methionyl-leucyl-phenylalanine (FMLP). The resting levels, as well as (Ca2+)i changes induced by FMLP in CGD cells, were quantitatively and kinetically similar to those observed in normal cells. We conclude that the defect in CGD cells is distal to, or independent of, the changes in (Ca2+)i induced by FMLP stimulation and that normal membrane depolarization does not seem to be necessary for receptor-mediated rise in free cytosolic calcium in human neutrophils.

scholarly journals Poly-arginine-18 (R18) Confers Neuroprotection through Glutamate Receptor Modulation, Intracellular Calcium Reduction, and Preservation of Mitochondrial Function

Molecules ◽  
2020 ◽  
Vol 25 (13) ◽  
pp. 2977
Author(s):  
Gabriella MacDougall ◽  
Ryan S. Anderton ◽  
Amy Trimble ◽  
Frank L. Mastaglia ◽  
Neville W. Knuckey ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Glutamate Receptor ◽  
Cortical Neurons ◽  
Calcium Influx ◽  
Ros Generation ◽  
Neuronal Cultures ◽  
Atp Production ◽  
Endoplasmic Reticulum Calcium ◽  
Receptor Modulation ◽  
Insight Into

Recent studies have highlighted that a novel class of neuroprotective peptide, known as cationic arginine-rich peptides (CARPs), have intrinsic neuroprotective properties and are particularly effective anti-excitotoxic agents. As such, the present study investigated the mechanisms underlying the anti-excitotoxic properties of CARPs, using poly-arginine-18 (R18; 18-mer of arginine) as a representative peptide. Cortical neuronal cultures subjected to glutamic acid excitotoxicity were used to assess the effects of R18 on ionotropic glutamate receptor (iGluR)-mediated intracellular calcium influx, and its ability to reduce neuronal injury from raised intracellular calcium levels after inhibition of endoplasmic reticulum calcium uptake by thapsigargin. The results indicate that R18 significantly reduces calcium influx by suppressing iGluR overactivation, and results in preservation of mitochondrial membrane potential (ΔΨm) and ATP production, and reduced ROS generation. R18 also protected cortical neurons against thapsigargin-induced neurotoxicity, which indicates that the peptide helps maintain neuronal survival when intracellular calcium levels are elevated. Taken together, these findings provide important insight into the mechanisms of action of R18, supporting its potential application as a neuroprotective therapeutic for acute and chronic neurological disorders.

scholarly journals Modulation of Endoplasmic Reticulum Calcium Pump Expression during T Lymphocyte Activation

1997 ◽  
Vol 272 (16) ◽  
pp. 10746-10750 ◽  
Author(s):  
Sophie Launay ◽  
Régis Bobe ◽  
Christine Lacabaratz-Porret ◽  
Raymonde Bredoux ◽  
Tünde Kovàcs ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
T Lymphocyte ◽  
Lymphocyte Activation ◽  
Calcium Pump ◽  
Endoplasmic Reticulum Calcium ◽  
T Lymphocyte Activation

Heterologous expression of polycystin-1 inhibits endoplasmic reticulum calcium leak in stably transfected MDCK cells

2008 ◽  
Vol 294 (6) ◽  
pp. F1279-F1286 ◽  
Author(s):  
Kimberly H. Weber ◽  
Eun Kyung Lee ◽  
Uma Basavanna ◽  
Sabina Lindley ◽  
Roy C. Ziegelstein ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Release ◽  
Mdck Cells ◽  
Calcium Ionophore ◽  
Calcium Flux ◽  
Calcium Stores ◽  
Endoplasmic Reticulum Calcium ◽  
Calcium Indicator ◽  
Luminal Calcium ◽  
Er Membrane

We previously found that polycystin-1 accelerated the decay of ligand-activated cytoplasmic calcium transients through enhanced reuptake of calcium into the endoplasmic reticulum (ER; Hooper KM, Boletta A, Germino GG, Hu Q, Ziegelstein RC, Sutters M. Am J Physiol Renal Physiol 289: F521–F530, 2005). Calcium flux across the ER membrane is determined by the balance of active uptake and passive leak. In the present study, we show that polycystin-1 inhibited calcium leak across the ER membrane, an effect that would explain the capacity of this protein to accelerate clearance of calcium from the cytoplasm following a calcium release response. Calcium leak was detected by measurement of the accumulation of calcium in the cytoplasm following treatment with thapsigargin. Heterologous polycystin-1, stably expressed in Madin-Darby canine kidney cells, attenuated the thapsigargin-induced calcium peak with no effect on basal calcium stores, mitochondrial calcium uptake, or extrusion of calcium across the plasma membrane. The capacity of polycystin-1 to limit the rate of decay of ER luminal calcium following inhibition of the pump was shown indirectly using the calcium ionophore ionomycin, and directly by loading the ER with a low-affinity calcium indicator. We conclude that disruption of ER luminal calcium homeostasis may contribute to the cyst phenotype in autosomal dominant polycystic kidney disease.

scholarly journals Elucidation of a TRPC6-TRPC5 Channel Cascade That Restricts Endothelial Cell Movement

2008 ◽  
Vol 19 (8) ◽  
pp. 3203-3211 ◽  
Author(s):  
Pinaki Chaudhuri ◽  
Scott M. Colles ◽  
Manjunatha Bhat ◽  
David R. Van Wagoner ◽  
Lutz Birnbaumer ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Calcium Concentration ◽  
Transient Receptor Potential ◽  
Calcium Influx ◽  
Cell Movement ◽  
Receptor Potential ◽  
Receptor Activation ◽  
Calcium Stores ◽  
Trpc Channels ◽  
Transient Receptor

Canonical transient receptor potential (TRPC) channels are opened by classical signal transduction events initiated by receptor activation or depletion of intracellular calcium stores. Here, we report a novel mechanism for opening TRPC channels in which TRPC6 activation initiates a cascade resulting in TRPC5 translocation. When endothelial cells (ECs) are incubated in lysophosphatidylcholine (lysoPC), rapid translocation of TRPC6 initiates calcium influx that results in externalization of TRPC5. Activation of this TRPC6–5 cascade causes a prolonged increase in intracellular calcium concentration ([Ca2+]i) that inhibits EC movement. When TRPC5 is down-regulated with siRNA, the lysoPC-induced rise in [Ca2+]i is shortened and the inhibition of EC migration is lessened. When TRPC6 is down-regulated or EC from TRPC6−/− mice are studied, lysoPC has minimal effect on [Ca2+]i and EC migration. In addition, TRPC5 is not externalized in response to lysoPC, supporting the dependence of TRPC5 translocation on the opening of TRPC6 channels. Activation of this novel TRPC channel cascade by lysoPC, resulting in the inhibition of EC migration, could adversely impact on EC healing in atherosclerotic arteries where lysoPC is abundant.

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