Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.5.4.4 (adenosine deaminase)
 5,136 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although infectious, inflammatory and neoplastic diseases frequently involve the pleural space and walls, little is known about the immunological and molecular mechanisms underlying pleural disorders. This article provides an overview of recent insights into immunobiological processes likely to play a role in the pathogenesis of pleural disorders. Pleural involvement in certain diseases is associated with the infiltration of a number of different types of immune cells, such as neutrophils, eosinophils or lymphocytes, in various proportions depending on both the course and the aetiology of the underlying disease. In addition to infiltrating cells, mesothelial cells have been demonstrated to actively participate in pleural inflammation via release of various mediators and proteins, including platelet-derived growth factor (PDGF), interleukin-8, monocyte chemotactic peptide (MCP-1), nitric oxide (NO), collagen, antioxidant enzymes and the plasminogen activation inhibitor (PAI). Furthermore, several inflammatory mediators have been detected at increased concentrations within pleural effusions, including lipid mediators, cytokines and proteins (adenosine deaminase, lysosyme, eosinophil-derived cationic proteins, and products of the coagulation cascade). The presence of these mediators underline the concept of pleural inflammation, and certain cytokines seem to characterize a specific aetiology of pleurisy. The understanding of these processes and the sequence of events leading to pleural loculation, pleural adhesion or repair are likely to provide the basis for early therapeutic intervention and reduce pleural-associated morbidity.
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PMID:Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy. 938 73

Here we describe properties of the P2-purinoceptor, which is involved in the regulation of the key enzyme of estrogen biosynthesis, aromatase cytochrome P-450, in stromal cells from human adipose tissue. Aromatase activity induced by cortisol and platelet-derived growth factor BB (PDGF-BB) is further increased by addition of ATP, ADP, AMP and, albeit with reduced potency, adenosine, GTP and adenosine(5')tetraphospho(5') adenosine. Stable P1-purinoceptor agonists are inactive, whereas P2X-purinoceptor agonists mimic the effects of purine(s) (nucleotides). Prior incubation of cells with a P2-purinoceptor antagonist, but not P1-purinoceptor antagonists, blocks augmentation of aromatase activity by all ligands. Nucleotides, but not adenosine, retain their ability to augment aromatase activity in the presence of adenosine deaminase, indicating that they do not act via their metabolite adenosine. These results lead to the conclusion, that at least one member of the P2-subclass of purinoceptors exists in adipose tissue and is involved in modulation of aromatase activity in vitro. The pharmacological profile of the P2-site differs from those reported for cloned P2-purinoceptors, but is similar to that of the P2X-subclass. Therefore, a combined response of different members of the P2X-purinoceptor subclass or of members of different P2-purinoceptor subclasses cannot be discounted. Purinoceptor activation triggers cytoplasmic calcium transients, which, in contrast to aromatase induction, are independent from the presence of cortisol and PDGF-BB. Therefore the involved P2-purinoceptor(s) seem(s) to be constitutively expressed in human adipose tissue stromal cells. P2-purinoceptor(s) might provide a direct link between sympathetic nerve activity and estrogen biosynthesis in human adipose tissue. Furthermore it (or they) may contribute to the regulation of lipolysis.
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PMID:Induction of aromatase activity in human adipose tissue stromal cells by extracellular nucleotides--evidence for P2-purinoceptors in adipose tissue. 952 24