Effect of cyclic adenosine monophosphate elevations on functional responses of polymorphonuclear leukocytes from patients with cystic fibrosis

1989 ◽  
Vol 6 (4) ◽  
pp. 237-241
Author(s):  
Susanne Suter ◽  
Isabelle Chevallier ◽  
Karl H. Krause ◽  
Daniel P. Lew
Keyword(s):  
Cystic Fibrosis ◽  
Polymorphonuclear Leukocytes ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Functional Responses

scholarly journals Platelet activation in cystic fibrosis

Blood ◽  
2005 ◽  
Vol 105 (12) ◽  
pp. 4635-4641 ◽  
Author(s):  
Brian P. O'Sullivan ◽  
Matthew D. Linden ◽  
Andrew L. Frelinger ◽  
Marc R. Barnard ◽  
Michele Spencer-Manzon ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Platelet Aggregation ◽  
Platelet Activation ◽  
Platelet Reactivity ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Gene Encoding ◽  
Platelet Surface ◽  
Beneficial Effects ◽  
Plasma Factor

Abstract Cystic fibrosis (CF) is caused by a mutation of the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). We examined platelet function in CF patients because lung inflammation is part of this disease and platelets contribute to inflammation. CF patients had increased circulating leukocyte-platelet aggregates and increased platelet responsiveness to agonists compared with healthy controls. CF plasma caused activation of normal and CF platelets; however, activation was greater in CF platelets. Furthermore, washed CF platelets also showed increased reactivity to agonists. CF platelet hyperreactivity was incompletely inhibited by prostaglandin E1 (PGE1). As demonstrated by Western blotting and reverse-transcriptase-polymerase chain reaction (RT-PCR), there was neither CFTR nor CFTR-specific mRNA in normal platelets. There were abnormalities in the fatty acid composition of membrane fractions of CF platelets. In summary, CF patients have an increase in circulating activated platelets and platelet reactivity, as determined by monocyte-platelet aggregation, neutrophil-platelet aggregation, and platelet surface P-selectin. This increased platelet activation in CF is the result of both a plasma factor(s) and an intrinsic platelet mechanism via cyclic adenosine monophosphate (cAMP)/adenylate cyclase, but not via platelet CFTR. Our findings may account, at least in part, for the beneficial effects of ibuprofen in CF. (Blood. 2005;105:4635-4641)

Cystic fibrosis

2011 ◽  
Author(s):  
R. Mark Beattie ◽  
Anil Dhawan ◽  
John W.L. Puntis
Keyword(s):  
Cystic Fibrosis ◽  
Clinical Symptoms ◽  
Gastrointestinal Symptoms ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Transmembrane Conductance Regulator ◽  
Transmembrane Conductance ◽  
Regulator Protein ◽  
Salt And Water Balance ◽  
Cystic Fibrosis Transmembrane

Gastrointestinal manifestations 156Management of gastrointestinal symptoms in children with CF 158Nutrition in CF 158Nutritional management 159Vitamins 160The incidence of cystic fibrosis (CF) is around 1 in 2500. Cases are diagnosed as a consequence of population screening or high-risk screening, or following presentation with clinical symptoms typical of the disorder. The basic defect is in the CFTR (cystic fibrosis transmembrane conductance regulator) protein which codes for a cyclic adenosine monophosphate-regulated chloride transporter in epithelial cells of exocrine organs. This is involved in salt and water balance across epithelial surfaces. The gene is on chromosome 7. There are multiple known mutations, the most common being ...

scholarly journals Studying signal compartmentation in adult cardiomyocytes

2020 ◽  
Vol 48 (1) ◽  
pp. 61-70 ◽  
Author(s):  
Aleksandra Judina ◽  
Julia Gorelik ◽  
Peter T. Wright
Keyword(s):  
Fluorescent Dyes ◽  
Fluorescent Proteins ◽  
Cyclic Adenosine Monophosphate ◽  
Adenosine Monophosphate ◽  
Cell Types ◽  
Functional Responses ◽  
Relative Contribution ◽  
New Perspective ◽  
Active Processes ◽  
Cell To Cell Variability

Multiple intra-cellular signalling pathways rely on calcium and 3′–5′ cyclic adenosine monophosphate (cAMP) to act as secondary messengers. This is especially true in cardiomyocytes which act as the force-producing units of the cardiac muscle and are required to react rapidly to environmental stimuli. The specificity of functional responses within cardiomyocytes and other cell types is produced by the organellar compartmentation of both calcium and cAMP. In this review, we assess the role of molecular localisation and relative contribution of active and passive processes in producing compartmentation. Active processes comprise the creation and destruction of signals, whereas passive processes comprise the release or sequestration of signals. Cardiomyocytes display a highly articulated membrane structure which displays significant cell-to-cell variability. Special attention is paid to the way in which cell membrane caveolae and the transverse-axial tubule system allow molecular localisation. We explore the effects of cell maturation, pathology and regional differences in the organisation of these processes. The subject of signal compartmentation has had a significant amount of attention within the cardiovascular field and has undergone a revolution over the past two decades. Advances in the area have been driven by molecular imaging using fluorescent dyes and genetically encoded constructs based upon fluorescent proteins. We also explore the use of scanning probe microscopy in the area. These techniques allow the analysis of molecular compartmentation within specific organellar compartments which gives researchers an entirely new perspective.

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