The Role of Organelles in Regulating Cytoplasmic Calcium in Vascular Smooth Muscle1

2015 ◽  
pp. 21-29 ◽  
Author(s):  
Andrew P. Somlyo
Keyword(s):  
Cytoplasmic Calcium

Albumin modulation of capillary permeability: role of endothelial cell [Ca2+]i

1993 ◽  
Vol 265 (1) ◽  
pp. H74-H82 ◽  
Author(s):  
P. He ◽  
F. E. Curry
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Calcium Concentration ◽  
Capillary Permeability ◽  
Common Mechanism ◽  
Cytoplasmic Calcium ◽  
Adsorption Model ◽  
Endothelial Cell Surface ◽  
Mesenteric Microvessels

Albumin is required in vascular perfusates to maintain the normal permeability of microvessel walls. The most common mechanism proposed for action of albumin involves binding to the endothelial cell surface to increase the resistance to water and solute flows through hydraulic pathways across the capillary wall. The results of the present experiments do not conform to this simple adsorption model. Ringer perfusion increased the hydraulic conductivity (Lp) of the wall of single perfused frog mesenteric microvessels by 4.0 +/- 0.5-fold. The increase in Lp was associated with an increase of cytoplasmic calcium concentration ([Ca2+]i) from 59 +/- 5 nM when albumin was in the perfusate to a transient peak of 181 +/- 13 nM, 1–2 min after Ringer perfusion. [Ca2+]i then fell back to close to 100 nM. Processes that reduced Ca2+ influx into endothelial cells (removal of extracellular Ca2+, membrane depolarization) reduced Ca2+ influx and attenuated the increase in [Ca2+]i. The same processes abolished the increase in Lp after Ringer perfusion and restored Lp to close to control values during Ringer perfusion. Thus Ca2+ entry into endothelial cells is required to initiate and maintain the increased permeability during Ringer perfusion.

The role of cytoplasmic calcium in the regulation of the resting potential in the pulmonary veins myocardium in rats and mice

2016 ◽  
Vol 469 (1) ◽  
pp. 152-155 ◽  
Author(s):  
V. M. Karimova ◽  
V. S. Kuzmin ◽  
N. A. Undrovinas ◽  
L. V. Rozenshtraukh
Keyword(s):  
Pulmonary Veins ◽  
Resting Potential ◽  
Cytoplasmic Calcium ◽  
Rats And Mice

scholarly journals Human T-Cell Lymphotropic Virus Type 1 p12I Expression Increases Cytoplasmic Calcium To Enhance the Activation of Nuclear Factor of Activated T Cells

2002 ◽  
Vol 76 (20) ◽  
pp. 10374-10382 ◽  
Author(s):  
Wei Ding ◽  
Björn Albrecht ◽  
Robert E. Kelley ◽  
Natarajan Muthusamy ◽  
Seung-Jae Kim ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Calcium Release ◽  
Nuclear Factor ◽  
Cytoplasmic Calcium ◽  
Activated T Cells ◽  
Human T Cell ◽  
Nfat Activation

ABSTRACT Human T-cell lymphotropic virus type 1 (HTLV-1) establishes persistent infection and is associated with lymphoproliferative or neurodegenerative diseases. As a complex retrovirus, HTLV-1 contains typical structural and enzymatic genes, as well as regulatory and accessory genes encoded in the pX region. The early events necessary for HTLV-1 to establish infection in lymphocytes, its primary target cells, remain unresolved. Recent studies have demonstrated the importance of regulatory and accessory gene products in determining this virus-host interaction. Among these, pX open reading frame I, which encodes two proteins, p12I and p27I, is required for establishing persistent infection in vivo and for infection in quiescent primary lymphocytes. In addition, p12I localizes in the endoplasmic reticulum (ER) and cis-Golgi apparatus and associates with a calcium binding protein, calreticulin. We recently reported that p12I expression induces the calcium-responsive T-cell transcription factor, nuclear factor of activated T cells (NFAT), in the presence of phorbol ester activation. Based on these studies, we hypothesize that p12I may modulate calcium release from the ER. Here, we report that p12I expression increases basal cytoplasmic calcium and concurrently diminishes calcium available for release from the ER stores. Overexpression of calreticulin, a calcium buffer protein, blocked p12I-mediated NFAT activation independently of its ability to bind p12I. Chemical inhibition studies using inhibitors of inositol 1,4,5-triphosphate receptor and calcium release-activated calcium channels suggest that inositol 1,4,5-triphosphate receptor in the ER membrane and calcium release-activated calcium channels in the plasma membrane contribute to p12I-mediated NFAT activation. Collectively, our results are the first to demonstrate the role of p12I in elevating cytoplasmic calcium, an antecedent to T-cell activation, and further support the important role of this accessory protein in the early events of HTLV-1 infection.

scholarly journals Synergism of platelet-aggregating agents. Role of elevation of cytoplasmic calcium.

1987 ◽  
Vol 80 (1) ◽  
pp. 267-271 ◽  
Author(s):  
J A Ware ◽  
M Smith ◽  
E W Salzman
Keyword(s):  
Cytoplasmic Calcium

Role of CD2 cross-linking in cytoplasmic calcium responses and T cell activation

1988 ◽  
Vol 18 (10) ◽  
pp. 1601-1608 ◽  
Author(s):  
Jeffrey A. Ledbetter ◽  
Peter S. Rabinovitch ◽  
Ingegerd Hellström ◽  
Karl Erik Hellström ◽  
Laura S. Grosmaire ◽  
...  
Keyword(s):  
T Cell ◽  
T Cell Activation ◽  
Cell Activation ◽  
Cross Linking ◽  
Cytoplasmic Calcium
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