Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00790 (PGA)
 2,475 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study mechanisms underlying selective enzyme release from human leukocytes during phagocytosis, the effects were studied of compounds which affect microtubule integrity or the accumulation of cyclic nucleotides. Human leukocytes selectively extrude lysosomal enzymes (beta-glucuronidase) from viable cells during phagocytosis of zymosan or immune complexes, or upon encounter with immune complexes dispersed along a non-phagocytosable surface such as a millipore filter. In each circumstance, lysosomal enzyme release was reduced by previous treatment of cells with pharmacological doses of drugs which disrupt microtubules (e.g. 10(-3)-10(-5) M colchicine) or with agents which affect accumulation of adenosine 3'5'-monophosphate (cAMP) (e.g. 10(-3) M cyclic nucleotides and 2.8 x 10(-4)-2.8 x 10(-6) M prostaglandin E (PGE) and A (PGA) compounds). Preincubation of cells with 5 microg/ml cytochalasin B resulted in complete inhibition of zymosan ingestion, but not of adherence of zymosan particles to plasma membranes or selective enzyme release. In this system, in which enzyme release was independent of particle uptake, preincubation of cells with colchicine, vinblastine, dibutyryl cAMP, or PGE(1) also reduced extrusion of lysosomal enzymes. When cell suspensions were incubated with membrane-lytic crystals of monosodium urate (MSU), cytoplasmic as well as lysosomal enzymes were released with subsequent death of the cells. However, enzyme release followed phagocytosis of crystals (as measured by enhanced C-1 oxidation of glucose) and was due to "perforation from within" of the lysosomal membrane, rather than lysis by crystals of the plasma membrane. Enzyme release after MSU ingestion was also reduced when cells were treated with pharmacological doses of the test agents. When cells were killed by Triton X-100, acting on the plasma membrane, C-1 oxidation of glucose was abolished and enzyme release could not be inhibited pharmacologically. These observations suggest that lysosomal enzyme release from human phagocytes can be an active process which accompanies plasma membrane stimulation, is independent of cell death, and may be controlled by cyclic nucleotides and agents which affect microtubules.
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PMID:Mechanisms of lysosomal enzyme release from human leukocytes. I. Effect of cyclic nucleotides and colchicine. 412 73

Polyglycolide (PGA) and chitosan mixture solution was prepared using solvents of low toxicity to create novel, porous, biocompatible, degradable, and modifiable hybrid matrices for biomedical applications. The porosity of these PGA-chitosan hybrid matrices (P/C matrices) was created by a thermally induced phase separation method. Two types of the P/C hybrid matrices containing 70 wt% PGA (P/C-1 matrix) and 30 wt% PGA (P/C-2 matrix) were fabricated. Chitosan matrix was also prepared for comparison. A 35-day in vitro degradation revealed that the weight losses for the P/C-1 and P/C-2 matrices were similar ( approximately 61%), but the releases of glycolic acid from the P/C-1 and P/C-2 matrices were 95% and 60%, respectively. The P/C-1 matrix had higher porosity and higher mechanical strength than the P/C-2 and chitosan matrices. Fibroblast cells cultivated in these matrices proliferated well and the cell density was the highest in the P/C-1 matrix, followed by the chitosan and P/C-2 matrices, suggesting good biocompatibility for the P/C-1 matrix. We thereby concluded that the P/C-1 matrix, due to its high strength, porosity, biocompatibility and degradability, is a promising biomaterial. The presence of chitosan in the P/C matrices provides many amino groups for further modifications such as biomolecule conjugation and thus enhances the application potential of the P/C hybrid matrices in tissue engineering.
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PMID:Fabrication of a novel porous PGA-chitosan hybrid matrix for tissue engineering. 1250 27