Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It has been reported that omental fat tissue is a good source of human microvascular endothelial cells. By characterization we demonstrate that the epitheloid cells isolated from omental tissue are not endothelial cells, but mesothelial cells. They contain abundant cytokeratins 8 and 18, which are absent in endothelial cells, and vimentin. No staining with the endothelial-specific antibodies EN-4 and PAL-E is observed. A faint and diffuse staining of von Willebrand factor (vWF) is seen in mesothelial cells, whereas microvascular endothelial cells from subcutaneous fat display vWF in distinct granular structures. Human peritoneal mesothelium produces plasminogen activator-dependent fibrinolytic activity, which is essential in the resolution of fibrous exudates and may therefore be important in preventing the formation of fibrous peritoneal adhesions. This fibrinolytic activity is plasminogen activator-dependent, but has not been fully characterized. We report here that human omental tissue mesothelial cells in vitro produce large amounts of tissue-type plasminogen activator (t-PA), together with type 1 and 2 plasminogen activator inhibitor (PAI-1 and PAI-2). PAI-1 is predominantly secreted into the culture medium, whereas the major part of PAI-2 is found in the cells. No urokinase-type plasminogen activator is detected. On stimulation with the inflammatory mediator tumor necrosis factor (TNF), at least a threefold decrease in t-PA antigen is observed, together with an increase in both PAI-1 and PAI-2. TNF also induces a marked change in cell shape. Whereas TNF and bacterial lipopolysaccharide (LPS) have similar effects on the production of PA inhibitor by human endothelial cells, LPS has no or only a relatively small effect on the fibrinolytic properties of mesothelial cells. The decreased fibrinolytic activity induced by the cytokine TNF may impair the natural dissolution of fibrin deposits at the peritoneum in the presence of an inflammatory reaction.
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PMID:Characterization and fibrinolytic properties of human omental tissue mesothelial cells. Comparison with endothelial cells. 210 84

Oxidative modification of low-density lipoproteins (LDLs) plays a key role in the development of atherosclerosis and the onset of coronary artery disease. LDL oxidation alters the antithrombotic balance of human endothelial cells inducing surface tissue factor (TF) pathway activity, which results in enhanced fibrin deposition. Fibrinolysis, which is strictly regulated by plasminogen activator inhibitor-1 (PAL-1) and tissue-type plasminogen activator (tPA). Is also dysregulated by LDL oxidation with a net increase in the inhibitory rate. Oxidized LDLs (oxLDLs) also affect many aspects of macrophage function linked to the inflammatory response of these cells, In particular, oxLDLs downregulate inducible cyclooxigenase (Cox-2) in human monocyte-derived macrophages exposed to bacterial lipopolysaccharide. This observation may support the hypothesis that, within atheromata, the transformation macrophages into foam cells results in the attenuation of the inflammatory response, thus contributing to the progression of athrogenesis. Among lipid constituents of oxLDLs, Ox-PAPC, a mixture of oxidized arachidonic acid-containing phospholipids, prevents Cox-2 expression, suggesting that it could be considered responsible for the biological activity of oxLDLs.
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PMID:Oxidized LDLs influence thrombotic response and cyclooxygenase 2. 1232 37

The objective of this research was to carry out an in vitro and in vivo study of the biological performance of PLLA/beta-TCP composite materials, to estimate the scope of their potential applications in bone surgery. Samples with increasing beta-TCP (0-60% w/w) contents were processed by injection molding. The in vitro study consisted of an evaluation of inflammatory potential by assaying the IL-1alpha secreted by monocytes, and then cell proliferation (counting) and phenotype expression (PAL and I collagen) in human osteogenous cells. The in vivo study was carried out using cylindrical implants of composite materials composed of composite materials containing 0 or 60% beta-TCP and pure beta-TCP, respectively. The implants were inserted in femoral sites in rabbits, using the Kathagen protocol. Each animal received a 60% implant, with either a 0 or a 100% implant in the contralateral femur, so that the materials could be compared with one another. Five animals were examined for each material and implantation period, giving a total of 30 animals. This study showed that adding increasing percentages of beta-TCP to a lactic acid polymer matrix stimulated the proliferation of human osteogenous cells and synthesis of the extracellular bone matrix in a dose-dependent manner. In vivo results indicate that, in comparison with pure PLA, tricalcium phosphate-containing composite materials had faster degradation kinetics, caused less inflammatory reaction, and promoted contact osteogenesis. The composite material containing 60% beta-TCP demonstrated a similar performance to pure tricalcium phosphate bone grafts in terms of osteogenesis, and is apparently compatible with the production of intra-osseous implants for situations representing high levels of mechanical strain.
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PMID:Biological performance of a new beta-TCP/PLLA composite material for applications in spine surgery: in vitro and in vivo studies. 1672 99

Polycystic ovary syndrome (PCOS) is a common endocrinological disorder in female reproductive age. Insulin resistance (IR) and compensatory hyperinsulinemia seem to be the main pathophysiologies of this syndrome. Therefore, PCOS is at risk for abnormal glucose tolerance, dyslipidemia, central obesity and hypertension. Also, plasminogen activator-inhibitor-1 (PAL-1), hemostatic factor and C-reactive protein (CRP), inflammatory factor have been reported in PCOS women. The metabolic syndrome (MS), a clustering of several metabolic abnormalities, is more prevalent in PCOS. One-third to 46% of PCOS women with MS have been reported. Since these metabolic abnormalities as well as MS are the important risk factors of cardiovascular disease (CVD), PCOS is at risk for CVD.
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PMID:Polycystic ovary syndrome and the metabolic syndrome. 2121 22

Plasminogen activator-plasmin system is the central role for thrombus degradation. The system is finely tuned to allow healing of a blood vessel lesion without compromising the stability of the fibrin thrombus, and to localize fibrinolytic activity to the damaged area. There is a dynamic balance between fibrinolytic factors (plasminogen activators and plasmin) and inhibitory proteins (PAL-1, alpha2-plasmin inhibitor, and TAFIa). An alternative pathway for fibrinolysis that comprises leukocyte elastase and its interaction with the plasminogen activator-plasmin system has been suggested.
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PMID:[Plasminogen activation and regulation of fibrinolysis]. 2516 11