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)

Using a biochemical technique, the authors characterized and identified a plasminogen activator (PA) derived from tissue extracts of antrochoanal polyp (AP) and paranasal mucous membrane (PMM) with chronic sinusitis. The results of fibrin zymography indicated that the tissue extracts of AP revealed two lytic zones and that those of PMM revealed a single lytic zone on fibrin-agarose plates. One of the AP zones exhibited the same relative mobility as the PMM zone (molecular weight: 65 kd), while the other AP zone had a smaller molecular weight (about 54 kd). Goat immunoglobulin G (IgG) fraction of antihuman uterine tissue-type plasminogen activator (t-PA) inhibited the 65-kd lytic zones of AP and PMM. Antihuman low-molecular-weight urokinase inhibited only the 54-kd lytic zone of AP, and nonspecific goat IgG failed to inhibit any of the lytic zones. On the other hand, 10(-2) mol trans 4-(aminomethyl)cyclohexane-carboxylic acid (t-AMCHA) inhibited all of the lytic zones. No lytic zones could be observed on plasminogen-free fibrin-agarose plates. These findings confirmed that the tissue extracts of PMM contained t-PA, and that those of AP contained both t-PA and urokinase-type plasminogen activator (u-PA). In addition, it appeared that u-PA in inflammatory tissue was related to proliferative changes of the mucous membrane.
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PMID:Presence of urokinase-type plasminogen activator (u-PA) in tissue extracts of antrochoanal polyp. 151 51

It is known that a remarkable fibrinolytic activity of plasminogen activator (PA) can be seen in extracts of wet tissue and acetone powder preparation of paranasal mucous membrane evidencing chronic sinusitis. However, the origin of the PA in extract of paranasal mucous membrane has not yet been clarified up to the present time. In this experiment, using a tissue culture of paranasal mucous membrane, it was observed that two species of cells, epithelial cells and fibrocytes, proliferated in the implanted tissue. PA was isolated from the conditioned medium on the fifth day after culture. From these results, it appears that the PA may be released from epithelial cells and/or fibroblasts.
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PMID:Fibrinolytic activity in medium from tissue culture of paranasal mucous membrane. 311 47

It is known that large amounts of plasminogen activator (PA) are contained in tissue extracts of the human paranasal mucous membrane (PMM) with chronic sinusitis. The present study was undertaken to isolate and purify the PA in tissue extracts of PMM. Furthermore, the purified PA was identified as to whether it was of the tissue type or urokinase (UK) type, and some of its fibrinolytic characteristics were determined in comparison with those of urokinase. As starting material, extracts of acetone powder of PMM with chronic sinusitis were used, and Zn-imminodiacetate affinity chromatography, and ultrafiltration were carried out to separate and purify the PA from the PMM. The PA was purified to a 107-fold increase in specific activity. The molecular weight of the PA was estimated to be 65,000 to 70,000 d by gel filtration using Sephacryl S-200. The purified PA was stable in the range of pH 8.0 to 9.0. Using S-2288, a synthetic substrate, the Michaelis constant (Km) of the purified PA was estimated to be 0.11 mmol. The binding of the purified PA to fibrin was stronger than that of UK, while the fibrinogenolytic activity of the purified PA was not stronger than that of UK. Based on these results, the purified PA was identified as a tissue-type plasminogen activator (t-PA). From the kinetic data, it was identified as being of the two-chain variety. It is considered that, as a thrombolytic agent, t-PA derived from the PMM could be more useful than UK.
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PMID:Fibrin binding, fibrinolytic and fibrinogenolytic activity of plasminogen activator derived from the paranasal mucous membrane of humans. 842 13

Chronic rhinosinusitis (CRS) is one of the most common chronic diseases in adults and severely affects quality of life in patients. Although various etiologic and pathogenic mechanisms of CRS have been proposed, the causes of CRS remain uncertain. Abnormalities in the coagulation cascade may play an etiologic role in many diseases, such as asthma and other inflammatory conditions. While studies on the relationship between asthma and dysregulated coagulation have been reported, the role of the coagulation system in the pathogenesis of CRS has only been considered following recent reports. Excessive fibrin deposition is seen in nasal polyp (NP) tissue from patients with chronic rhinosinusitis with nasal polyp (CRSwNP) and is associated with activation of thrombin, reduction of tissue plasminogen activator (t-PA) and upregulation of coagulation factor XIII-A (FXIII-A), all events that can contribute to fibrin deposition and crosslinking. These findings were reproduced in a murine model of NP that was recently established. Elucidation of the mechanisms of fibrin deposition may enhance our understanding of tissue remodeling in the pathophysiology of NP and provide new targets for the treatment of CRSwNP.
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PMID:Chronic Rhinosinusitis and the Coagulation System. 2612 2