NITRIC OXIDE, FREE RADICALS AND CELL SIGNALLING IN CARDIOVASCULAR DISEASE

1997 ◽  
Vol 25 (3) ◽  
pp. 384S-384S
Author(s):  
Victor M. Darley-Usmar ◽  
Joanne McAndrew ◽  
Roger White ◽  
Rakesh Patel ◽  
Doug Moellering ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Free Radicals ◽  
Cell Signalling

Nitric oxide, free radicals and cell signalling in cardiovascular disease

1997 ◽  
Vol 25 (3) ◽  
pp. 925-929 ◽  
Author(s):  
V. M. Darley-Usmar ◽  
J. McAndrew ◽  
R. Patel ◽  
D. Moellering ◽  
T. M. Lincoln ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease ◽  
Free Radicals ◽  
Cell Signalling

scholarly journals Nitric Oxide and Cardiovascular Disease

1995 ◽  
Vol 2 (3) ◽  
pp. 73-79
Author(s):  
Motoyuki Nakamura ◽  
Katsuhiko Hiramori
Keyword(s):  
Nitric Oxide ◽  
Cardiovascular Disease

Subversion of host cell signalling by the protozoan parasiteLeishmania

Parasitology ◽  
2005 ◽  
Vol 130 (S1) ◽  
pp. S27-S35 ◽  
Author(s):  
D. J. GREGORY ◽  
M. OLIVIER
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cell Signalling ◽  
Protein Tyrosine Phosphatases ◽  
Innate Immune ◽  
Signalling Pathways ◽  
Oxygen Species ◽  
Obligate Intracellular ◽  
Intracellular Parasites ◽  
Intracellular Ca

The protozoaLeishmaniaspp. are obligate intracellular parasites that inhabit the macrophages of their host. Since macrophages are specialized for the identification and destruction of invading pathogens, both directly and by triggering an innate immune response,Leishmaniahave evolved a number of mechanisms for suppressing some critical macrophage activities. In this review, we discuss how various species ofLeishmaniadistort the host macrophage's own signalling pathways to repress the expression of various cytokines and microbicidal molecules (nitric oxide and reactive oxygen species), and antigen presentation. In particular, we describe how MAP Kinase and JAK/STAT cascades are repressed, and intracellular Ca2+and the activities of protein tyrosine phosphatases, in particular SHP-1, are elevated.

Cell-type specific calcium signalling in a Drosophila epithelium

1997 ◽  
Vol 110 (15) ◽  
pp. 1683-1692 ◽  
Author(s):  
P. Rosay ◽  
S.A. Davies ◽  
Y. Yu ◽  
A. Sozen ◽  
K. Kaiser ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Critical Role ◽  
Cell Signalling ◽  
Calcium Signalling ◽  
Malpighian Tubule ◽  
Fluid Secretion ◽  
Cell Types ◽  
Cytosolic Calcium ◽  
Atpase Inhibitor ◽  
Principal Cells

Calcium is a ubiquitous second messenger that plays a critical role in both excitable and non-excitable cells. Calcium mobilisation in identified cell types within an intact renal epithelium, the Drosophila melanogaster Malpighian tubule, was studied by GAL4-directed expression of an aequorin transgene. CAP2b, a cardioactive neuropeptide that stimulates fluid secretion by a mechanism involving nitric oxide, causes a rapid, dose-dependent rise in cytosolic calcium in only a single, genetically-defined, set of 77 principal cells in the main (secretory) segment of the tubule. In the absence of external calcium, the CAP2b-induced calcium response is abolished. In Ca2+-free medium, the endoplasmic reticulum Ca2+-ATPase inhibitor, thapsigargin, elevates [Ca2+]i only in the smaller stellate cells, suggesting that principal cells do not contain a thapsigargin-sensitive intracellular pool. Assays for epithelial function confirm that calcium entry is essential for CAP2b to induce a physiological response in the whole organ. Furthermore, the data suggest a role for calcium signalling in the modulation of the nitric oxide signalling pathway in this epithelium. The GAL4-targeting system allows general application to studies of cell-signalling and pharmacology that does not rely on invasive or cytotoxic techniques.

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