Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The therapy with thymus extracts, oral and parenteral, reduced the frequency and the intensity of recurrences of herpes labialis infections. The duration of the effect was at least 6 month after interruption of the therapy. Indomethacin was effective and developed and intensive effect only during the therapy. The skin test with recall-antigens and the neopterin-elimination were altered at the first day of the menstruation during the recurrence. The normalisation succeeded during therapy. In patients with recurrences in the perimenstrual time we observed a reduced T-helper/T-suppressor index during the first day of menstruation. Normal data were registered out of the recurrence time and/or under therapy. Inhibitors of the lymphokine: leucocyte/migration inhibitory factor (LIF) with a molecular weight of 6-12 KD were obtained with the specific stimulation of mononuclear cells of patients with recurrent infections with herpes labialis using the herpes-virus-1 antigen. The inhibition of fibrinolysis/proteolysis with aprotinin, tranexamic acid, phenyl-methyl-sulphonyl-fluoride and di-isopropyl-fluorophosphate could prevent the appearance of inhibitors. Inhibitors could be produced by splitting the LIF-molecule with urokinase and plasminogen but not with trypsin. The production, but not the activity, of present LIF-inhibitors are blocked in vivo and in vitro by indomethacin and thymus peptides.
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PMID:[Recurrent herpes labialis infections: cellular immunity and immunomodulation]. 253 31

Although Mycobacterium avium is usually nonpathogenic in healthy individuals, in vitro infection of macrophages (M phi) from the majority of healthy donors induces death of the cells 2 wk after infection; this effect is in contrast to noninfected M phi, which survive for months in culture. We demonstrate here that treatment of normal M phi with indomethacin further shortens the life of these cells to 48 h after infection with M. avium. Indomethacin treatment of the M phi also prevents M. avium-dependent accumulation of mRNA-encoding plasminogen activator inhibitor type-2 (PAI-2), an inhibitor of urokinase-type plasminogen activator. Occurrence of nuclear condensation and DNA fragmentation in M phi pretreated with indomethacin and infected with M. avium indicates that the early death of these cells is caused by apoptosis. In contrast, priming of M phi with GM-CSF significantly prolongs their survival after M. avium infection and enhances M. avium-induced accumulation of PAI-2 mRNA. Most importantly, addition of PAI-2 is sufficient to prevent apoptosis of M phi infected with M. avium in the presence of indomethacin. Finally, M phi not treated with indomethacin also die of apoptosis 7 to 10 days after M. avium infection and can be rescued by PAI-2. These studies indicate that production of PAI-2 by normal M phi as a consequence of M. avium infection inhibits programmed cell death, a mechanism that might serve to prevent the spread of the infection.
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PMID:Plasminogen activator inhibitor type 2 prevents programmed cell death of human macrophages infected with Mycobacterium avium, serovar 4. 763 97

Endometrial stromal cells from rat uteri differentially sensitized for the decidual cell reaction in vivo and which undergo differing degrees of decidualization in vitro were cultured and plasminogen activator (PA) in the medium determined. The cells were obtained by enzymatic dispersion from the uteri of ovariectomized, steroid-treated rats at the equivalent of day 4, 5, or 6 of pseudopregnancy or on day 5 from rats treated on day 4 with 0, 0.3, or 1.0 microgram estradiol (low, intermediate, or high dose of estradiol, respectively) and cultured for 24, 48, or 72 hr. For cells from day 4, 5, and 6 uteri cultured under control conditions, PA activity in the medium was greatest for day 5 cells, which were from uteri maximally sensitized for decidualization both in vivo and in vitro. By contrast, for cells from low-, intermediate-, and high-estradiol uteri, PA activity in the medium was greatest for the high-estradiol cells; these cells do not undergo decidualization in vivo or in vitro to the same extent as intermediate-estradiol cells. Indomethacin, an inhibitor of prostaglandin (PG) synthesis, reduced PGE2 accumulation to nondetectable amounts and for most cultures decreased PA activity in the medium, suggesting that endogenous PG production regulated in part PA secretion under control conditions. The addition of PGE2 with indomethacin increased PA activities above those under control conditions, but activities were still lower for day 4 and 6 cells compared with day 5 cells, and for low- and intermediate-estradiol cells compared with high-estradiol cells. This indicates that the differences in PA secretion are not explainable by differences in PGE2 production. Northern blot analysis of RNA from cells cultured for 72 hr under control conditions did not reveal significant differences in steady-state concentrations of mRNA for urokinase-type PA or plasminogen activator inhibitor 1, but those for tissue-type PA were lower in day 6 cells compared with day 4 and 5 cells. It is concluded that PA activity secreted by the cultured endometrial stromal cells, although controlled in part by the endocrine milieu to which they were exposed prior to culture, does not simulate decidualization in vitro and, therefore, that PA activity is not a marker for decidualization in vitro.
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PMID:Secretion of plasminogen activator by cultured rat endometrial stromal cells from uteri differentially sensitized for the decidual cell reaction. 949 79

The effect of epidermal growth factor (EGF) on the accumulation of plasminogen activator (PA) activity in the medium of cultured rat endometrial stromal cells isolated from uteri sensitized for the decidual cell reaction was examined. Treatment with EGF increased, in a concentration-dependent manner, PA activity in the medium. This effect was inhibited or greatly reduced by inhibitors of transcription and translation. Incubation of the cells with prostaglandin E2 increased PA activity in the medium. Indomethacin, which inhibited prostaglandin accumulation in the medium, slightly but significantly decreased the EGF-induced increase in PA activity in the medium. As indicated by zymography and the use of amiloride in the PA assay, the activity in the medium was primarily urokinase-type plasminogen activator (uPA). Finally, EGF caused an increase in the steady-state uPA mRNA levels in the cells. These results provide evidence that EGF causes an increase in the secretion of uPA by rat endometrial stromal cells from uteri sensitized for the decidual cell reaction through a mechanism that involves an increase in steady-state uPA mRNA levels.
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PMID:Regulation of plasminogen activator in rat endometrial stromal cells: the role of epidermal growth factor. 954 11