Activation of endoplasmic reticulum calcium leak by 2-APB depends on the luminal calcium concentration

Cell Calcium ◽  
2017 ◽  
Vol 65 ◽  
pp. 80-90 ◽  
Author(s):  
Daniel Leon-Aparicio ◽  
Jesus Chavez-Reyes ◽  
Agustin Guerrero-Hernandez
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Concentration ◽  
Endoplasmic Reticulum Calcium ◽  
Luminal Calcium

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 Selenoprotein N is an endoplasmic reticulum calcium sensor that links luminal calcium levels to a redox activity

2020 ◽  
Vol 117 (35) ◽  
pp. 21288-21298 ◽  
Author(s):  
Alexander Chernorudskiy ◽  
Ersilia Varone ◽  
Sara Francesca Colombo ◽  
Stefano Fumagalli ◽  
Alfredo Cagnotto ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Single Amino Acid ◽  
Redox Activity ◽  
Calcium Stores ◽  
Calcium Sensor ◽  
Oligomeric State ◽  
Endoplasmic Reticulum Calcium ◽  
Ef Hand ◽  
Luminal Calcium ◽  
Er Calcium

The endoplasmic reticulum (ER) is the reservoir for calcium in cells. Luminal calcium levels are determined by calcium-sensing proteins that trigger calcium dynamics in response to calcium fluctuations. Here we report that Selenoprotein N (SEPN1) is a type II transmembrane protein that senses ER calcium fluctuations by binding this ion through a luminal EF-hand domain. In vitro and in vivo experiments show that via this domain, SEPN1 responds to diminished luminal calcium levels, dynamically changing its oligomeric state and enhancing its redox-dependent interaction with cellular partners, including the ER calcium pump sarcoplasmic/endoplasmic reticulum calcium ATPase (SERCA). Importantly, single amino acid substitutions in the EF-hand domain of SEPN1 identified as clinical variations are shown to impair its calcium-binding and calcium-dependent structural changes, suggesting a key role of the EF-hand domain in SEPN1 function. In conclusion, SEPN1 is a ER calcium sensor that responds to luminal calcium depletion, changing its oligomeric state and acting as a reductase to refill ER calcium stores.

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 Hepatic endoplasmic reticulum calcium fluxes: effect of free fatty acids and KATP channel involvement

2021 ◽  
Vol 41 (2) ◽  
Author(s):  
Rawan Al-Rawi ◽  
Xudong Wang ◽  
Kenneth McCormick
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Influx ◽  
Calcium Flux ◽  
Calcium Efflux ◽  
Biochemical Processes ◽  
Endoplasmic Reticulum Calcium ◽  
Hepatic Microsomes ◽  
High Calcium ◽  
Luminal Calcium ◽  
Noxious Effect

Abstract As a common sequel to obesity, plasma and intracellular free fatty acid (FFA) concentrations are elevated and, as a consequence, manifold disturbances in metabolism may ensue. Biochemical processes in the cytosol and organelles, such as mitochondria and endoplasmic reticulum (ER), can be disturbed. In the ER, the maintenance of a high calcium gradient is indispensable for viability. In sarcoplasmic reticulum, selective FFA can induce ER stress by disrupting luminal calcium homeostasis; however, there are limited studies in hepatic microsomes. Our studies found that FFA has a noxious effect on rat hepatic microsomal calcium flux, and the extent of which depended on the number of double bonds and charge. Furthermore, insofar as the FFA had no effect on microsomal calcium efflux, their inhibitory action primarily involves calcium influx. Finally, other cationic channels have been found in hepatic ER, and evidence is presented of their interaction with the Ca2+ ATPase pump.

Sarco-Endoplasmic Reticulum Calcium Release Model Based on Changes in the Luminal Calcium Content

2019 ◽  
pp. 337-370 ◽  
Author(s):  
Agustín Guerrero-Hernández ◽  
Víctor Hugo Sánchez-Vázquez ◽  
Ericka Martínez-Martínez ◽  
Lizeth Sandoval-Vázquez ◽  
Norma C. Perez-Rosas ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Release ◽  
Calcium Content ◽  
Endoplasmic Reticulum Calcium ◽  
Model Based ◽  
Luminal Calcium ◽  
Release Model

scholarly journals Bid agonist regulates murine hepatocyte proliferation by controlling endoplasmic reticulum calcium homeostasis

Hepatology ◽  
2010 ◽  
Vol 52 (1) ◽  
pp. 338-348 ◽  
Author(s):  
Hong-Min Ni ◽  
Catherine J. Baty ◽  
Na Li ◽  
Wen-Xing Ding ◽  
Wentao Gao ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Homeostasis ◽  
Hepatocyte Proliferation ◽  
Endoplasmic Reticulum Calcium ◽  
Murine Hepatocyte

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
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