Disease relevance of PGG

• We have isolated the cDNA for both human platelet and human erythroleukemia cell PGG/H synthase using the polymerase chain reaction and conventional screening procedures [1].
• These results suggest that the protective effect exhibited by PGG glucan in the rat peritonitis model is mediated, at least in part, by prostaglandins [2].
• The increased in vivo thromboxane A2 generation existing in these patients and the selective sensitivity of erythromelalgia to aspirin suggest that platelet PGG/H synthase products may be involved in transducing the increased thrombotic risk [3].
• Reduction of infection-stimulated periapical bone resorption by the biological response modifier PGG glucan [4].
• Cyclooxygenases (COX, prostaglandin endoperoxide synthases, PGG/H synthases) are potent mediators of edema, impeding blood flow and immunomodulation in the pathologically altered brain [5].

High impact information on PGG

• M-CSF-induced MO, in sharp contrast, expressed little PGG/H synthase protein, mRNA, cellular enzyme activity, or PGE2 release, despite comparable levels of cellular PLA2 activity [6].
• Cellular PGG/H synthase (cyclooxygenase) levels were quantified by cytometric analysis with antibodies specific for the two isozymes of PGG/H synthase (PGG/H synthases 1 and 2) [6].
• The levels of PGE2 converted were quantitated by radioimmunoassay (RIA). mRNA levels of the enzymes were detected by Northern blot analysis hybridized with mouse PGG/H synthase cDNA probes, 2.7 kb (PGG/H synthase 1) and 4.2 kb (PGG/H synthase 2) [6].
• The PGG/H synthase gene was assigned to chromosome 9 by analysis of a human--hamster somatic hybrid DNA panel [1].
• Platelet-derived growth factor and phorbol ester differentially regulated the expression of PGG/H synthase mRNA levels in the megakaryocytic/platelet-like HEL cell line [1].

Biological context of PGG

• The effect of PGG-beta-glucan on neutrophil chemotaxis in vivo [7].
• Prostaglandin synthesis is controlled by cyclooxygenases (COX, prostaglandin endoperoxide synthase, PGG/H synthase) and COX expression has been attributed a key role in immunomodulation, hemostasis and inflammation in a wide variety of pathologically altered brain tissues [8].
• A study of PGG and EGG waveforms correlated with videostroboscopy in an in-vivo canine model of phonation with simulated unilateral recurrent or superior laryngeal nerve paralysis is presented [9].
• The aspirin and heme binding sites of PGG/H synthase [10].

Anatomical context of PGG

• Fibroblast growth factor upregulates PGG/H synthase in rabbit microvascular endothelial cells by a glucocorticoid independent mechanism [11].
• Acidic FGF treatment of aspirin treated endothelial cells from rabbit lung microvessels and small pulmonary artery and from human lung microvessels all showed an increase in PGG/H synthase recovery [11].
• Quantitative studies of leukocytes of rats and mice following a single injection of PGG glucan showed a modest transient increase in the total leukocyte count [12].
• Serum induction and superinduction of PGG/H synthase mRNA levels in 3T3 fibroblasts [13].

Associations of PGG with other chemical compounds

• 13CH2-multiplet nuclear magnetic resonance relaxation studies on proline (P)-containing glycine (G)-based peptides, GP, PG, GPG, PGG, and GPGG, provided numerous dipolar auto- and cross-correlation times for various motional model analyses of backbone and proline-ring bond rotations [14].

Gene context of PGG

• The N-terminal hinge was mutated to P166/V167G/W168G (PGG), and the C-terminal hinge was mutated to K174G/T175G/A176G (GGG) in chicken TIM [15].
• In addition, the actions of aFGF on de novo PGG/H synthase were compared in several endothelial preparations [11].
• PGG/H synthase synthesis following aspirin treatment was also increased by transforming growth factor beta, while epidermal growth factor basic FGF and platelet derived growth factor were without effect [11].

References