Calcium content of the endoplasmic reticulum of snail neurones releasable by caffeine

Cell Calcium ◽  
2013 ◽  
Vol 53 (2) ◽  
pp. 120-124 ◽  
Author(s):  
Roger C. Thomas
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Content ◽  
Snail Neurones

scholarly journals Protective effect of endoplasmic reticulum stress on calcification of VSMCs induced by high glucose and its effect on expression of GRP78, CHOP, and Caspase-12

2019 ◽  
Vol 17 ◽  
pp. 205873921985760
Author(s):  
Jingping Xu ◽  
Dawei Wu ◽  
Xiaoli Li ◽  
Haiying Zhu ◽  
Xu Teng ◽  
...  
Keyword(s):  
Alkaline Phosphatase ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Phosphatase Activity ◽  
Alkaline Phosphatase Activity ◽  
High Glucose ◽  
Calcium Content ◽  
Bone Differentiation ◽  
High Glucose Group ◽  
Glucose Group

This article investigates the role of endoplasmic reticulum stress (ERS) in high-glucose-induced vascular smooth muscle cells (VSMCs) calcification and to explore its effects on the expression of GRP78, CHOP, and Caspase-12.VSMCs were treated with high glucose (35 mmoL/L) to induce diabetes to see whether high glucose can induce ERS. Changes in alkaline phosphatase activity, calcium deposition, and runt-related transcription factor 2 (Runx2) were measured. After 5 days’ treatment, the alkaline phosphatase activity, calcium content, and Runx2 expression of the bone differentiation marker protein were all up-regulated in the β-glycerophosphate group, the high-glucose group, and the β-glycerophosphate + high-glucose group when compared with the control group. High-glucose treatment of VSMCs can cause ERS and apoptosis and induces transdifferentiation of VSMCs into osteoblast-like cells, resulting in increased basal phosphatase activity, up-regulation of calcium content, and bone differentiation markers in VSMCs. The findings confirm that ERS plays an important role in the calcification of VSMCs.

Role of endoplasmic reticulum calcium content in prostate cancer cell growth regulation by IGF and TNFalpha

2004 ◽  
Vol 201 (2) ◽  
pp. 201-213 ◽  
Author(s):  
Sandrine Humez ◽  
Gillaume Legrand ◽  
Fabien Vanden-Abeele ◽  
Micha�l Monet ◽  
Philipe Marchetti ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Endoplasmic Reticulum ◽  
Cell Growth ◽  
Cancer Cell ◽  
Growth Regulation ◽  
Prostate Cancer Cell ◽  
Calcium Content ◽  
Cancer Cell Growth ◽  
Endoplasmic Reticulum Calcium

scholarly journals Calcium homoeostasis modulator 1 (CALHM1) reduces the calcium content of the endoplasmic reticulum (ER) and triggers ER stress

2011 ◽  
Vol 437 (3) ◽  
pp. 469-475 ◽  
Author(s):  
Sonia Gallego-Sandín ◽  
María Teresa Alonso ◽  
Javier García-Sancho
Keyword(s):  
Endoplasmic Reticulum ◽  
Plasma Membrane ◽  
Er Stress ◽  
Disease Risk ◽  
Cell Damage ◽  
Binding Protein ◽  
Simian Virus 40 ◽  
Calcium Content ◽  
Simian Virus ◽  
T Antigen

CALHM1 (calcium homoeostasis modulator 1), a membrane protein with similarity to NMDA (N-methyl-D-aspartate) receptor channels that localizes in the plasma membrane and the ER (endoplasmic reticulum) of neurons, has been shown to generate a plasma-membrane Ca2+ conductance and has been proposed to influence Alzheimer's disease risk. In the present study we have investigated the effects of CALHM1 on intracellular Ca2+ handling in HEK-293T [HEK (human embryonic kidney)-293 cells expressing the large T-antigen of SV40 (simian virus 40)] cells by using targeted aequorins for selective monitorization of Ca2+ transport by organelles. We find that CALHM1 increases Ca2+ leak from the ER and, more importantly, reduces ER Ca2+ uptake by decreasing both the transport capacity and the Ca2+ affinity of SERCA (sarcoplasmic/endoplasmic reticulum Ca2+-ATPase). As a result, the Ca2+ content of the ER is drastically decreased. This reduction in the Ca2+ content of the ER triggered the UPR (unfolded protein response) with induction of several ER stress markers, such as CHOP [C/EBP (CCAAT/enhancer-binding protein)-homologous protein], ERdj4, GRP78 (glucose-regulated protein of 78 kDa) and XBP1 (X-box-binding protein 1). Thus CALHM1 might provide a relevant link between Ca2+ homoeostasis disruption, ER stress and cell damage in the pathogenesis of neurodegenerative diseases

Downregulation of AβPP Enhances Both Calcium Content of Endoplasmic Reticulum and Acidic Stores and the Dynamics of Store Operated Calcium Channel Activity

2013 ◽  
Vol 34 (2) ◽  
pp. 407-415 ◽  
Author(s):  
Maria Chatzistavraki ◽  
Elli Kyratzi ◽  
Angeliki Fotinopoulou ◽  
Panagiota Papazafiri ◽  
Spiros Efthimiopoulos
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Channel ◽  
Calcium Content ◽  
Channel Activity

Calcium content of mitochondria and endoplasmic reticulum in liver frozen rapidly in vivo

Nature ◽  
1985 ◽  
Vol 314 (6012) ◽  
pp. 622-625 ◽  
Author(s):  
A. P. Somlyo ◽  
Meredith Bond ◽  
Avril V. Somlyo
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Content
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