Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.7 (plasmin)
 9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The uterus of the pig secretes large amounts of protein in response to progesterone. Estrogen alone has little effect but in combination with progesterone is synergistic at low doses and inhibitory at high doses. The responses of the uterus to progesterone require prolonged hormone treatment and are not immediate. The proteins secreted by the uterus of all species are believed to play some role in the nutritional and developmental support of the conceptuses, particularly during early pregnancy. Such a role is likely to be of greater importance in species such as the pig which possesses a noninvasive, diffuse-type of epitheliochorial placentation. A group of basic polypeptides dominates the uterine secretions of the pig. The best characterized is uteroferrin, a purple colored, iron-containing acid phosphatase which transports iron across the placenta. Three polypeptides which are found associated noncovalently with uteroferrin have been shown to be antigenically closely related to each other and to have arisen from a single precursor polypeptide. Their function is unknown. A family of plasmin/trypsin inhibitors which show sequence homology with bovine pancreatic trypsin inhibitor (aprotinin) has been well characterized and appears to control intrauterine proteolytic events initiated by the conceptuses. Several other proteins secreted in response to progesterone remain to be characterized and functionally defined.
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PMID:Hormonal control and function of secretory proteins. 345 17

In Vienna, Austria, health workers took blood samples from 16 healthy, nonsmoking 19-35 year old women before and after they began using a combined oral contraceptive (OC) (Gynovin) (30 mcg ethinyl estradiol and 75 mcg gestodene) to assess the OC's effects on blood coagulation and fibrinolysis and the effect of the estrogen component on endothelial cells. Fibrinogen levels increased significantly after OC use (283 mg/dl vs. 342 mg/dl after the 1st treatment cycle; p .005). These levels remained significantly higher (326 mg/dl and 339 mg/dl after the 2nd and 3rd treatment cycles; p .005 and .05, respectively). Thrombin antithrombin III complex (TAT) and prothrombin fragment F1+2 levels increased just minimally during OC treatment. Levels of fibrin split-product D-dimer, plasma tissue plasminogen activator (t-PA) activity, and plasmin-antiplasmin (PAP) complexes were significantly higher during all OC treatment cycles than they were before treatment. Active plasminogen activator inhibitor (PAI-1) antigen, t-PA, and urokinase plasminogen activator antigen levels fell significantly after OC treatment and remained low during OC treatment. Experiments with the culture of human umbilical vein endothelial cells showed that ethinyl estradiol did not significantly affect the tissue factor content or surface thrombomodulin activity of these endothelial cells (i.e., hemostatic regulatory activities). It also did not change the secretion of the fibrinolytic components t-PA and PAI-1. None of the women developed thrombosis. Even though these findings did not clearly show OC-induced hemostatic activation in this relatively small group of women, clinical researchers should still determine activation markers to monitor the activation state of blood coagulation in certain OC users, such as obese women and those who smoke cigarettes.
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PMID:Studies on oral contraceptive-induced changes in blood coagulation and fibrinolysis and the estrogen effect on endothelial cells. 839 73

The purpose of this study was to evaluate whether the plasminogen and plasmin system within bovine mammary secretions was influenced by an estrogen treatment that was used to accelerate mammary tissue involution. Holstein cows were injected with 4 ml of ethanol excipient (n = 21) or 15 mg of estradiol-17 beta (n = 23) on each of the 4 d that preceded final milk removal. Dates of final milk removal (d 0) were designated as 60 d prior to expected dates of calving. Each mammary quarter was sampled once to collect secretions that corresponded to d 0, 3, 11, and 25 or d 1, 7, 18, and 30 of the dry period. Concentrations of plasminogen, plasmin, and somatic cells in secretions increased earlier for treated cows than for control cows. The ratio of plasminogen to plasmin in secretions decreased earlier for treated cows than for control cows. These responses support the suggestion that the plasminogen and plasmin system is involved in the involution of bovine mammary tissue. Estrogen treatment increased the activation of plasminogen, which was evidenced by a precipitous decrease in the ratio of plasminogen to plasmin that occurred as concentrations of plasminogen and plasmin increased. The activation of plasminogen likely contributed to the increased rate of mammary tissue involution that was effected by exogenous estrogen. Endogenous estrogen secreted by the developing fetal and placental unit might mediate, in part, the gradual involution that occurs during lactation.
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PMID:Milk plasmin during bovine mammary involution that has been accelerated by estrogen. 927 94

The risk of thromboembolic complications with the use of second and third generation oral contraceptives is minimal and probably related to underlying congenital or acquired thrombophilic states. Estrogen dose-dependency leads to increased thrombin generation and increased plasmin generation. There is no convincing evidence that the balance between clotting and fibrinolysis is disturbed. The risk of venous thromboembolism with pregnancy is greater than with oral contraceptives. Hormone replacement therapy is safe for healthy women, and the benefits far outweigh the potential risks.
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PMID:Oral contraceptive pills and hormonal replacement therapy and thromboembolic disease. 1100 33

The present study explored the effects of estrogen on transcervical tight-junctional resistance (R(TJ)) and the mechanisms involved. Treatment of cultured human cervical epithelial cells with 17beta-estradiol decreased in a time- and dose-related manner the R(TJ). Estrogen had no significant effect on the expression of E-Cadherin, zonula-occluden-1, or Claudin-4. In contrast, 17beta-estradiol modulated expression of the transmembrane tight-junctional protein occludin: at low concentrations (1 and 10 nm) estradiol increased the density of occludin 65-kDa form but at the higher concentration of 100 nm estradiol induced only a mild 2-fold increase in the density of this form. Estradiol also increased the expression of occludin 50-kDa form in a dose-related manner. The R(TJ) and occludin effects of estradiol were reversible and could be blocked by tamoxifen but not progesterone. The present results rule out estrogen modulation of occludin transcription. In contrast, the results suggest that the occludin effects of estrogen involve posttranslational up-regulation of occludin turnover, including synthesis and degradation. The effects of estrogen on occludin expression were compared with those of proteinase-K, plasmin, and matrix-metaloproteinase-2 (all added extracellularly). The three proteinases abrogated irreversibly the R(TJ) and induced expression de novo of occludin low-molecular-weight forms. The latter, however, differed from the effect of estrogen, which generated only a single 50-kDa form. Collectively, the present data suggest that the occludin 50-kDa form is an estrogen-specific-induced occludin isoform and that the mechanism of estrogen-abrogation of transcervical R(TJ) involves occludin modulation.
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PMID:Estrogen abrogates transcervical tight junctional resistance by acceleration of occludin modulation. 1547 19