Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.17 (lysozyme)
 21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

N-acetyl-beta-glucosaminidase (EC 3.2.1.30, recommended name beta-N-Acetylglucosaminidase) was found to be a constituent of human cardiac lysosomes. beta-glucuronidase was also found in this tissue, while lysozyme, an enzyme present in leucocyte lysosomes, was not detectable in the heart. The activities of both N-acetyl-beta-glucosaminidase and beta-glucuronidase were elevated in plasma during the first 24 h after the onset of chest pain in patients with acute myocardial infarction and the peak levels of N-acetyl-beta-glucosaminidase correlated well with those of creatine kinase. N-acetyl-beta-glucosaminidase showed a further rise in plasma activity which gave a peak at 72 h after the onset of chest pain and this was accompanied by a rise in lysozyme activity. It is suggested that lysosome disruption caused by myocardial cell necrosis was responsible for the initial rise in plasma lysosomal enzyme activity and that the subsequent inflammatory reaction gave rise to the second peak.
Cardiovasc Res 1978 Feb
PMID:Plasma lysosomal enzyme activity in acute myocardial infarction. 64 16

Phagocytic cells, such as polymorphonuclear neutrophils, monocytes, and macrophages, are essential for defense against infection caused by a variety of microorganisms. The mechanisms used by these cells to destroy microbes comprise a potent oxidative armamentarium including superoxide, hydrogen peroxide, and hypochlorous acid. In addition, granule contents such as proteolytic enzymes, lysozyme, lactoferrin, and myeloperoxidase are released into the phagosome to destroy ingested microorganisms. Inflammatory cytokines, such as tumor necrosis factor (TNF), interleukin-1 (IL-1), and IL-6, enhance the phagocytic and microbicidal activity of the cells and increase their stickiness. It has been demonstrated in a variety of animal and clinical studies that activated phagocytes can damage the host they are designed to protect, using the mechanisms described above. Alkylxanthines, including pentoxifylline, are potent inhibitors of this inflammatory damage by two major actions: (a) reduction of the production of inflammatory cytokines (especially TNF) by phagocytes stimulated with a variety of microbial products (e.g., endotoxin); and (b) reversal of the effect of these cytokines on phagocytes. Thus, pentoxifylline counteracts the following effects of inflammatory cytokines on phagocytes: increased adherence, shape change resulting in larger size and rigidity, increased oxidative burst, priming for an enhanced oxidative burst, increased degranulation, and decreased chemotactic movement. In addition, these activities synergize with the normal anti-inflammatory mediator adenosine. Alkylxanthines have the potential to be effective therapy for conditions in which inflammatory cytokines and phagocytes cause damage, including the sepsis syndrome, ARDS, AIDS, and arthritis.
J Cardiovasc Pharmacol 1995
PMID:Cytokines, phagocytes, and pentoxifylline. 869 56

Kawasaki disease is an acute vasculitis of unknown cause that occurs predominantly in infants and young children and produces coronary artery aneurysms in approximately 15% to 25% of those affected. In the United States, Kawasaki disease is more commonly the cause of noncongenital heart disease in children than is acute rheumatic fever. Therapy for Kawasaki disease in the acute phase is aimed at reducing inflammation of the coronary artery wall and preventing coronary thrombosis; treatment with high-dose intravenous gamma globulin and aspirin has become the standard of care and reduces the risk of development of coronary artery aneurysms by three- to fivefold. Even when treated with high-dose intravenous immune globulin G (IVIG) regimens within the first 10 days of illness, however, approximately 5% of children with Kawasaki disease develop at least transient coronary artery dilation, and 1% develop giant aneurysms. For those with persistent or recrudescent fever despite initial IVIG infusion, multiple courses of gamma globulin and treatment with cortico- steroids may be indicated. Early experience suggests that therapies aimed at reducing the amount of tumor necrosis factor alpha have a role. For those who develop coronary artery aneurysms, chronic antithrombotic regimens are instituted. When aneurysms are small or moderate in size, aspirin alone may be sufficient, but for patients with giant aneurysms, most experts choose to treat Kawasaki disease with aspirin plus warfarin. Acute coronary thromboses are treated with platelet IIb/IIIa antagonists and thrombolytic therapy. For children with coronary artery stenoses and consequent ischemic heart disease, the therapeutic armamentarium is similar to that used in adults with atherosclerotic coronary artery disease and includes coronary artery bypass grafting and transcatheter interventions.
Curr Treat Options Cardiovasc Med 2000 Jun
PMID:Kawasaki Disease. 1109 28

The mesangial cells of the glomerulus, the proximal tubular cells and the interstitial fibroblasts are the first choice targets for renal drug delivery since they play a pivotal role in many disease processes in the kidney. In the present review, only targeting to the proximal tubular cell is addressed because only this has been studied extensively. Two approaches of drug delivery to the proximal tubular cell have been studied up to now, the prodrug/softdrug and low-molecular-weight protein (LMPWP) approach. Most research on tubular specific drug delivery has focused on the development of amino-acid prodrugs that, after delivery, require activation by more or less kidney-selective enzymes. Large differences in renal selectivity are found. For some prodrugs, a rapid removal of the released drug from the kidney explained the low renal selectivity whereas for others, cleavage in non-target tissue and insufficient transport across the cell to the enzyme site seemed mainly responsible. The LMWP approach is based on drug attachment to a protein (<30 kD) that is freely filtered through the glomerulus and after accumulation is selectively catabolized in the lysosomes of the proximal tubular cell. Using LMWPs as drug carriers, a higher renal selectivity can be attained and a broader range of drugs can be attached while the rate of drug release can also be manipulated. The studies with captopril-lysozyme and naproxen-lysozyme clearly showed that targeting resulted in a higher renal selectivity and that drugs delivered into and regenerated in the proximal tubular cell exert renal selective pharmacological activity. Further testing will provide more definite data on the added value of this delivery technology.
Cardiovasc Drugs Ther 2002 Dec
PMID:Specific drug delivery to the kidney. 1279 65

The reliability of a rabbit polyclonal antibody against muramidase to identify monocytes/macrophages in swine was evaluated by immunostaining of cell smears and formaldehyde-fixed, paraffin-embedded tissue sections. Blood in tissue sections, cell smears (peripheral blood, buffy coat, and isolated mononuclear cells), and cultured mononuclear cells (adherent monocytes) contained positively stained cells with a morphology and in a number corresponding to that expected for a monocyte marker. Polymorphonuclear leukocytes (PMN), lymphocytes, and platelets were negative. In normal organs and tissues, mesenchymal cells with a distribution similar to that expected for macrophages were found to stain positively for muramidase. In pathologic tissues, positively stained inflammatory cells were identified in wounds, infected lungs, recently infarcted myocardium, and acute (variable numbers), organizing (often many), and healed (usually few) arterial thrombi. Enzymatic unmasking of antigenic determinants by trypsinization was necessary to achieve strong and consistent staining of monocytes/macrophages in tissue sections. A variety of epithelial cells of no differential diagnostic significance for monocyte/macrophage identification (e.g., renal proximal tubular cells) also stained positive for muramidase. The staining pattern of muramidase in swine corresponds to that described in humans, in whom muramidase has been shown to be a valuable marker of monocytes/macrophages. Swine PMN were, however, not stained or only weakly stained, whereas human PMN reportedly are strongly positive. As in humans, swine cardiac myocytes, smooth muscle cells, endothelial cells, lymphocytes, and platelets were consistently negative. This antibody against muramidase is a useful immunohistochemical marker for swine monocytes/macrophages in formaldehyde-fixed, paraffin-embedded tissues.
Cardiovasc Pathol
PMID:Muramidase: A useful monocyte/macrophage immunocytochemical marker in swine, of special interest in experimental cardiovascular disease. 2599 Sep 95