Effects of sulfonylureas on the synthesis and secretion of plasminogen activator from bovine aortic endothelial cells.

Kuo, Be-Sheng; Korner, Gil; Bjornsson, Thorir D.

doi:10.1172/jci113378

Cited by 20 publications

(25 citation statements)

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“…Chlorpropamide, for example, seems unique in promoting secretion of antidiuretic hormone and hence water retention (7). Some sulfonylureas might activate fibrinolysis (8), and there may be different (beneficial or harmful) effects of different sulfonylureas on the heart (3,9,10).…”

Section: Clinical Effect Differences Mainly Relate To Differences In mentioning

confidence: 99%

Kinetics-Effect Relations of Insulin-Releasing Drugs in Patients With Type 2 Diabetes

Melander

2004

Diabetes

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Sulfonylureas and glinides have similar mechanisms of action but differ in receptor affinity and binding sites and in absorption and elimination rates. This promotes differences in potency, rate of onset, and duration of action. While prominent in single-dose studies, these differences have less importance during long-term sulfonylurea treatment: at ordinary dosages, rapid-and short-acting (glipizide) and slow-and long-acting (glyburide) sulfonylureas maintained continuously effective plasma levels and similar 24-h glucose control. Moreover, there was no difference in patient outcome between the first-generation sulfonylurea chlorpropamide and the second-generation glyburide in the U.K. Prospective Diabetes Study. However, the risk of longlasting and hence dangerous hypoglycemia is higher with these two long-acting sulfonylureas. Conversely, this risk should be low with the short-acting glinides, but seemingly at the expense of less effective glucose control. The most important kinetics-effect relations are that hyperglycemia delays sulfonylurea absorption and that the sulfonylurea dose-response curve is bell shaped; continuous sulfonylurea exposure over a certain level (e.g., 10 mg glipizide) impairs rather than improves insulin and glucose responses to sulfonylurea (downregulation). Accordingly, a vicious circle may be established: unrelenting hyperglycemia may promote sulfonylurea dose increase, which increases hyperglycemia, promoting further dose increase and eventually therapeutic failure. Diabetes 53 (Suppl. 3):S151-S155, 2004

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Section: Clinical Effect Differences Mainly Relate To Differences In mentioning

confidence: 99%

Kinetics-Effect Relations of Insulin-Releasing Drugs in Patients With Type 2 Diabetes

Melander

2004

Diabetes

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“…Fibrin plate assay PA activity was determined on fibrin-coated, 96-well plates, using modification of previously described methods (Levin, 1983;Kuo et al, 1988). Briefly, the assay was performed in a final volume of 0.35 ml reaction mixture (0.1% gelatin in 1 mM EDTA, 100 mM Tris-HC1, pH 8.0) containing 1 pg plasminogen and the unknown or standard t-PA (1-20 mIU).…”

Section: Preparation Of Ecm-coated Dishesmentioning

confidence: 99%

“…Briefly, the assay was performed in a final volume of 0.35 ml reaction mixture (0.1% gelatin in 1 mM EDTA, 100 mM Tris-HC1, pH 8.0) containing 1 pg plasminogen and the unknown or standard t-PA (1-20 mIU). This mixture was incubated in a 96-well plate coated with 1.25 pg 1251-fibrin (17,000 cpm) per well, as described (Kuo et al, 1988). The plates were incubated for 2 h a t 37°C and the reaction mixture was then removed and counted for released radioactivity.…”

Section: Preparation Of Ecm-coated Dishesmentioning

confidence: 99%

“…In other experiments the ECM was partially solubilized by incubation (30 min, 37°C) with a minimal volume (0.1-0.2 m1135 mm dish) of a solution containing 1% SDS, 1 mM EDTA, and 25 mM Tris-HCI, pH 8.0, and the ECM was scraped from the dish. When 1% SDS treated samples were tested, they were first treated with 10% Triton X-100 for 30 min at 37°C (Kuo et al, 1988;Levin, 1983).…”

Section: Preparation Of Ecm-coated Dishesmentioning

confidence: 99%

“…SDS-PAGE zymography analysis PA activity was demonstrated by the polyacrylamide gel-zymography method (Heussen and Dowdle, 1980;Kuo et al, 1988) and performed on minigels of 60 x 90 x 15 mm in size. The 10% gels were copolymerized with 0.1% gelatin, 0.1 mgiml plasminogen, and 0.05 mg/ml fibrinogen.…”

Section: Preparation Of Ecm-coated Dishesmentioning

confidence: 99%

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Extracellular matrix produced by cultured corneal and aortic endothelial cells contains active tissue‐type and urokinase‐type plasminogen activators

Korner¹,

Bjornsson²,

Vlodavsky³

1993

Journal Cellular Physiology

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Incubation of plasminogen with the subendothelial extracellular matrix (ECM) synthesized by cultured bovine corneal and aortic endothelial cells resulted in generation of fibrinolytic activity, indicated by proteolysis of 125I-fibrin in a time- and dose-dependent manner. Both tissue-type plasminogen activator (t-PA) and urokinase-type plasminogen activator (u-PA) were identified in the ECM by fibrin zymography, immunoblotting, and inhibition of plasminogen activation by anti-u-PA and anti-t-PA antibodies. Most of the ECM-resident plasminogen activator (PA) activity did not originate from intracellular PA release occurring when the endothelial cells were lyzed and the ECM exposed, since a comparable amount of PA was associated with the ECM when the cells were lyzed with Triton X-100 or removed intact by treatment with 2 M urea. Active u-PA and t-PA were released from ECM by treatment with heparanase (endo-beta-D-glucuronidase), indicating that some of the ECM-resident PA activity is sequestered by heparan sulfate side chains. These results indicate that both u-PA and t-PA produced by endothelial cells are firmly sequestered in an active form by the subendothelial ECM. It is suggested that ECM-resident plasminogen activators participate in sequential matrix degradation during cell invasion and tumor metastasis. PA activity may also function in release of ECM-bound growth factors (i.e., basic fibroblast growth factor) and activation of proenzymes (i.e., prothrombin), resulting in modulation of the ECM growth-promoting and thrombogenic properties.

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Sulfonylureas: Basic Aspects and Clinical Uses

Melander¹

2004

International Textbook of Diabetes Mellitus

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This chapter describes the chemistry, mechanism of action, pharmacodynamics, pharmacokinetics, kinetics–effect relations, clinically beneficial and adverse effects of sulfonylurea drugs, as well as the efficacy of these agents in randomized‐controlled clinical trials and other studies. It also compares the different sulfonylurea compounds, especially in terms of differences in potency, rate of onset, and duration of action, and how such differences may contribute to different clinical profiles of the various compounds. In addition, some important interactions with other drugs are listed. Their appropriate place in the therapeutic armamentarium concerning type 2 diabetes is thoroughly discussed.

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Effects of sulfonylureas on the synthesis and secretion of plasminogen activator from bovine aortic endothelial cells.

Cited by 20 publications

References 35 publications

Kinetics-Effect Relations of Insulin-Releasing Drugs in Patients With Type 2 Diabetes

Kinetics-Effect Relations of Insulin-Releasing Drugs in Patients With Type 2 Diabetes

Extracellular matrix produced by cultured corneal and aortic endothelial cells contains active tissue‐type and urokinase‐type plasminogen activators

Sulfonylureas: Basic Aspects and Clinical Uses

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