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We began analyzing https://link.springer.com/article/10.1007/s00395-011-0233-5, but it redirected us to https://link.springer.com/article/10.1007/s00395-011-0233-5. The analysis below is for the second page.

Title[redir]:
Loss of DPP4 activity is related to a prothrombogenic status of endothelial cells: implications for the coronary microvasculature of myocardial infarction patients | Basic Research in Cardiology
Description:
Pro-coagulant and pro-inflammatory intramyocardial (micro)vasculature plays an important role in acute myocardial infarction (AMI). Currently, inhibition of serine protease dipeptidyl peptidase 4 (DPP4) receives a lot of interest as an anti-hyperglycemic therapy in type 2 diabetes patients. However, DPP4 also possesses anti-thrombotic properties and may behave as an immobilized anti-coagulant on endothelial cells. Here, we studied the expression and activity of endothelial DPP4 in human myocardial infarction in relation to a prothrombogenic endothelial phenotype. Using (immuno)histochemistry, DPP4 expression and activity were found on the endothelium of intramyocardial blood vessels in autopsied control hearts (n = 9). Within the infarction area of AMI patients (n = 73), this DPP4 expression and activity were significantly decreased, coinciding with an increase in Tissue Factor expression. In primary human umbilical vein endothelial cells (HUVECs), Western blot analysis and digital imaging fluorescence microscopy revealed that DPP4 expression was strongly decreased after metabolic inhibition, also coinciding with Tissue Factor upregulation. Interestingly, inhibition of DPP4 activity with diprotin A also enhanced the amount of Tissue Factor encountered and induced the adherence of platelets under flow conditions. Ischemia induces loss of coronary microvascular endothelial DPP4 expression and increased Tissue Factor expression in AMI as well as in vitro in HUVECs. Our data suggest that the loss of DPP4 activity affects the anti-thrombogenic nature of the endothelium.

Matching Content Categories {📚}

  • Education
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Custom-built

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🏙️ Massive Traffic: 50M - 100M visitors per month


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Many websites are intended to earn money, but some serve to share ideas or build connections. Websites exist for all kinds of purposes. This might be one of them. Doi.org could be secretly minting cash, but we can't detect the process.

Keywords {🔍}

dpp, tissue, factor, article, endothelial, cells, expression, google, scholar, pubmed, cas, inhibition, patients, platelets, activity, myocardial, fig, blood, control, coronary, infarction, ami, intramyocardial, vessels, human, huvecs, ros, diprotin, induced, shown, microvascular, effects, microvasculature, metabolic, heart, analysis, glp, arrows, van, microscopy, platelet, incubated, hearts, imaging, ischemia, size, phase, nuclear, role, reduced,

Topics {✒️}

ca2+-free krebs–ringer buffer long-term clinical outcome cleaving n-terminal gly-pro fibronectin-coated μ-slides vi0 substrate glycyl-proline-4-beta-naphthylamide 3d-digital imaging microscopy article download pdf possesses anti-thrombotic properties platelet-mediated myocardial injury histochemical azo-coupling reaction c-reactive protein colocalizes donkey-anti-mouse-alexa 488 donkey-anti-rabbit-alexa 647 dipeptidyl peptidase iv heat-inactivated human serum rabbit-anti-mouse-hrp microparticle-stimulated endothelial cells platelet adhesion-inducing tnfα pro-coagulant endothelial phenotype full size image pro-coagulant tissue factor di–iii tissue factor ischemia-induced tissue factor 19 mm tri-sodium citrate open access mentioned angiogenesis-inducing conversion pdgf receptor alpha/beta dipeptidyl peptidase-4 inhibition 20 mm 2-deoxy-d-glucose moonlighting protein cd26/dppiv digital imaging microscopy tissue factor/fviia complex acute myocardial infarction oxygen free radicals dpp4-positive blood vessels multiple comparison tests mediates platelet adhesion detected cd31-positive thrombi human myocardial infarction possibly ischemia-induced loss reduced intramyocardial coagulation imaging microvascular obstruction tissue factor induced platelet adhesion resulting full access privacy choices/manage cookies pro-coagulant state determine cell viability diprotin a-mediated effects vascular protective effects

Questions {❓}

  • Baidoshvili A, Krijnen PA, Kupreishvili K, Ciurana C, Bleeker W, Nijmeijer R, Visser CA, Visser FC, Meijer CJ, Stooker W, Eijsman L, van Hinsbergh VW, Hack CE, Niessen HW, Schalkwijk CG (2006) N(epsilon)-(carboxymethyl)lysine depositions in intramyocardial blood vessels in human and rat acute myocardial infarction: a predictor or reflection of infarction?
  • Baroldi G, Marzilli M, L’Abbate A, Arbustini E (1990) Coronary occlusion: cause or consequence of acute myocardial infarction?

Schema {🗺️}

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      headline:Loss of DPP4 activity is related to a prothrombogenic status of endothelial cells: implications for the coronary microvasculature of myocardial infarction patients
      description:Pro-coagulant and pro-inflammatory intramyocardial (micro)vasculature plays an important role in acute myocardial infarction (AMI). Currently, inhibition of serine protease dipeptidyl peptidase 4 (DPP4) receives a lot of interest as an anti-hyperglycemic therapy in type 2 diabetes patients. However, DPP4 also possesses anti-thrombotic properties and may behave as an immobilized anti-coagulant on endothelial cells. Here, we studied the expression and activity of endothelial DPP4 in human myocardial infarction in relation to a prothrombogenic endothelial phenotype. Using (immuno)histochemistry, DPP4 expression and activity were found on the endothelium of intramyocardial blood vessels in autopsied control hearts (n = 9). Within the infarction area of AMI patients (n = 73), this DPP4 expression and activity were significantly decreased, coinciding with an increase in Tissue Factor expression. In primary human umbilical vein endothelial cells (HUVECs), Western blot analysis and digital imaging fluorescence microscopy revealed that DPP4 expression was strongly decreased after metabolic inhibition, also coinciding with Tissue Factor upregulation. Interestingly, inhibition of DPP4 activity with diprotin A also enhanced the amount of Tissue Factor encountered and induced the adherence of platelets under flow conditions. Ischemia induces loss of coronary microvascular endothelial DPP4 expression and increased Tissue Factor expression in AMI as well as in vitro in HUVECs. Our data suggest that the loss of DPP4 activity affects the anti-thrombogenic nature of the endothelium.
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         Acute myocardial infarction
         Tissue Factor
         ROS
         Coagulation
         Platelet adhesion
         Cardiology
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