Faculty Opinions recommendation of Cyclic ADP-ribose production by CD38 regulates intracellular calcium release, extracellular calcium influx and chemotaxis in neutrophils and is required for bacterial clearance in vivo.

2002 ◽  
Author(s):  
Marcus Thelen
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Bacterial Clearance ◽  
Cyclic Adp Ribose ◽  
Intracellular Calcium Release

scholarly journals Genetic ablation of calcium-independent phospholipase A2β causes hypercontractility and markedly attenuates endothelium-dependent relaxation to acetylcholine

2010 ◽  
Vol 298 (6) ◽  
pp. H2208-H2220 ◽  
Author(s):  
Hans H. Dietrich ◽  
Dana R. Abendschein ◽  
Sung Ho Moon ◽  
Neema Nayeb-Hashemi ◽  
David J. Mancuso ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Extracellular Calcium ◽  
Genetic Ablation ◽  
Vasomotor Function ◽  
Intracellular Calcium Release

Activation of phospholipases leads to the release of arachidonic acid and lysophospholipids that play prominent roles in regulating vasomotor tone. To identify the role of calcium-independent phospholipase A2β (iPLA2β) in vasomotor function, we measured vascular responses to phenylephrine (PE) and ACh in mesenteric arterioles from wild-type (WT; iPLA2β+/+) mice and those lacking the β-isoform (iPLA2β−/−) both ex vivo and in vivo. Vessels isolated from iPLA2β−/− mice demonstrated increased constriction to PE, despite lower basal smooth muscle calcium levels, and decreased vasodilation to ACh compared with iPLA2β+/+ mice. PE constriction resulted in initial intracellular calcium release with subsequent steady-state constriction that depended on extracellular calcium influx. Endothelial denudation had no effect on vessel tone or PE-induced constriction although the dilation to ACh was significantly reduced in iPLA2β+/+ vessels. In contrast, vessels from iPLA2β−/− constricted by 54% after denudation, indicating smooth muscle hypercontractility. In vivo, blood pressure, resting vessel diameter, and constriction of mesenteric vessels to PE were not different in iPLA2β−/− vessels compared with WT mouse vessels. However, relaxation after ACh administration in situ was attenuated, indicating an endothelial inability to induce dilation in response to ACh. In cultured endothelial cells, inhibition of iPLA2β with ( S)-(E)-6-(bromomethylene)tetrahydro-3-(1-naphthalenyl)-2 H-pyran-2-one (BEL) decreased endothelial nitric oxide synthase phosphorylation and reduced endothelial agonist-induced intracellular calcium release as well as extracellular calcium influx. We conclude that iPLA2β is an important mediator of vascular relaxation and intracellular calcium homeostasis in both smooth muscle and endothelial cells and that ablation of iPLA2β causes agonist-induced smooth muscle hypercontractility and reduced agonist-induced endothelial dilation.

scholarly journals Calcium Influx, But Not Intracellular Calcium Release, Supports PACAP-Mediated ERK Activation in HEK PAC1 Receptor Cells

2014 ◽  
Vol 54 (3) ◽  
pp. 342-350 ◽  
Author(s):  
Victor May ◽  
Todd A. Clason ◽  
Thomas R. Buttolph ◽  
Beatrice M. Girard ◽  
Rodney L. Parsons
Keyword(s):  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Pac1 Receptor ◽  
Erk Activation ◽  
Receptor Cells ◽  
Intracellular Calcium Release

scholarly journals T cells deficient in inositol 1,4,5-trisphosphate receptor are resistant to apoptosis.

1997 ◽  
Vol 17 (6) ◽  
pp. 3005-3012 ◽  
Author(s):  
T Jayaraman ◽  
A R Marks
Keyword(s):  
T Cells ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Calcium Influx ◽  
Cell Receptor ◽  
Calcium Release Channel ◽  
Release Channel ◽  
Inositol 1,4,5 Trisphosphate ◽  
Intracellular Calcium Release ◽  
Trisphosphate Receptor

The type 1 inositol 1,4,5-trisphosphate receptor (IP3R1) calcium release channel is present on the endoplasmic reticulum of most cell types. T lymphocytes which have been made deficient in IP3R1 lack detectable IP3-induced intracellular calcium release and exhibit defective signaling via the T-cell receptor (TCR) (T. Jayaraman, E. Ondriasova, K. Ondrias, D. Harnick, and A. R. Marks, Proc. Natl. Acad. Sci. USA 92:6007-6011, 1995). We now show that IP3R1-deficient T cells are resistant to apoptosis induced by dexamethasone, TCR stimulation, ionizing radiation, and Fas. Resistance to TCR-mediated apoptosis in IP3R1-deficient cells is reversed by pharmacologically raising cytoplasmic calcium levels. TCR-mediated apoptosis can be induced in calcium-free media, indicating that extracellular calcium influx is not required. These findings suggest that intracellular calcium release via the IP3R1 is a critical mediator of apoptosis.

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