Feedback activation of factor XI by thrombin does not occur in plasma

bianjie submitted, created time 1 year 5 months (www.pnas.org)

In this study, we tested the hypothesis that factor XI (FXI) activation occurs in plasma following activation of the extrinsic pathway by thrombin-mediated feedback activation.

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Endogenous platelet factor 4 stimulates activated protein C generation in vivo and improves survival after thrombin or lipopolysaccharide challenge

addict submitted, created time 1 year 7 months (bloodjournal.hematologylibrary.org)

Pharmacologic infusion of activated protein C (APC) improves survival in severe sepsis, and platelet factor 4 (PF4) accelerates APC generation in a primate thrombin-infusion model. We now tested whether endogenous platelet PF4 content affects APC generation. Mice completely deficient in PF4 (mPF4-/-) had impaired APC generation and survival after thrombin infusion, similar to the impairment seen in heterozygote protein C-deficient (PC+/-) mice.

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Thrombin-initiated platelet activation in vivo is vWF independent during thrombus formation in a laser injury model

julie submitted, created time 1 year 8 months (www.jci.org)

"Adhesion of platelets to an injured vessel wall and platelet activation are critical events in the formation of a thrombus. Of the agonists involved in platelet activation, thrombin, collagen, and vWF are known to induce in vitro calcium mobilization in platelets. Using a calcium-sensitive fluorochrome and digital multichannel intravital microscopy to image unstimulated and stimulated platelets, calcium mobilization was monitored as a reporter of platelet activation (as distinct from platelet accumulation) during thrombus formation in live mice"

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Thrombin regulates intracellular cAMP concentration in human platelets through phosphorylation/activation of PDE3A

collapsar submitted, created time 1 year 9 months (bloodjournal.hematologylibrary.org)

Thrombin-induced cAMP reduction potentates several steps in platelet activation, including Ca++ mobilization, cytoskeletal reorganization, and fibrinogen receptor conformation. We now reinvestigate the signaling pathways by which intracellular cAMP content is controlled following platelet activation by thrombin. When washed human platelets were stimulated with thrombin, cAMP-dependent phosphodiesterase (PDE3A) activity was significantly increased

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Phospholipase A2 Activates Hemostasis

addict submitted, created time 1 year 9 months (la-press.com)

Phospholipases A2 (PLA2) are aggressive enzymes that can destroy phospholipids of cell membranes. The resulting cell fragments trigger the kallikrein—mediated contact phase of coagulation. The aim of the present study was to expose citrated whole blood to PLA2 and to quantify thrombin generation in recalcified plasma. The result shows elevated plasmatic PLA2 activities (occurring e.g. in trauma, pancreatitis, or sepsis) activate the blood hemostasis system resulting in pathologic disseminated intravascular coagulation (PDIC)

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