How Thrombomodulin Enables W215A/E217A Thrombin to Cleave Protein C but Not Fibrinogen

Biochemistry ◽  
2022 ◽  
Author(s):  
Riley B. Peacock ◽  
Taylor McGrann ◽  
Sofia Zaragoza ◽  
Elizabeth A. Komives
Keyword(s):  
Protein C

Activated protein C: the cure for sepsis - again?

Anaesthesia ◽  
2001 ◽  
Vol 56 (12) ◽  
pp. 1133-1135 ◽  
Author(s):  
Tariq Hoth ◽  
Timothy W. Evans
Keyword(s):  
Protein C ◽  
Activated Protein C

Homozygous mutation in ABCA3 Lipid-Transporter defect (EXON 9) and low level of surfactant protein C

2010 ◽  
Vol 222 (S 01) ◽  
Author(s):  
J Pöschl ◽  
P Ruef ◽  
M Griese ◽  
P Lohse ◽  
C Aslanidis ◽  
...  
Keyword(s):  
Protein C ◽  
Surfactant Protein ◽  
Homozygous Mutation ◽  
Surfactant Protein C ◽  
Low Level ◽  
Exon 9 ◽  
Lipid Transporter

Coagulation Factor V Leiden Mutation Was Detected in the Patients with Activated Protein C Resistance in Thailand

1998 ◽  
Vol 80 (08) ◽  
pp. 344-345 ◽  
Author(s):  
Pasra Arnutti ◽  
Motofumi Hiyoshi ◽  
Wichai Prayoonwiwat ◽  
Oytip Nathalang ◽  
Chamaiporn Suwanasophon ◽  
...  
Keyword(s):  
Protein C ◽  
Activated Protein C ◽  
Factor V Leiden ◽  
Coagulation Factor ◽  
Factor V ◽  
Activated Protein C Resistance ◽  
Factor V Leiden Mutation ◽  
Coagulation Factor V

Alveolar dynamics and beyond – The importance of surfactant protein C in cholesterol metabolism and lung homeostasis

2018 ◽  
Author(s):  
J Ruwisch ◽  
N Roldan ◽  
J Perez-Gil ◽  
TE Weaver ◽  
M Ochs ◽  
...  
Keyword(s):  
Protein C ◽  
Cholesterol Metabolism ◽  
Surfactant Protein ◽  
Surfactant Protein C

High Levels of Circulating Thrombomodulin in Human Foetuses and Children

1999 ◽  
Vol 81 (06) ◽  
pp. 906-909 ◽  
Author(s):  
Marie-Hélène Aurousseau ◽  
Danielle Gozin ◽  
Fernand Daffos ◽  
Armando D’Angelo ◽  
François Forestier ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Endothelial Cell ◽  
Protein C ◽  
Endothelial Cell Surface ◽  
A Value ◽  
Median Level ◽  
Group A ◽  
Anticoagulant Function ◽  
Cell Surface Proteoglycan ◽  
Human Foetuses

SummaryThrombomodulin (TM) is an endothelial cell surface proteoglycan with anticoagulant functions, also implicated in cell proliferation, cell-cell adhesion and differentiation. In this study we determined circulating plasma TM (pTM) levels in human foetuses at different stages of pregnancy, at birth and in childhood. TM levels increased with gestational age, the median level reaching a peak of approximately 165 ng/ml between the 23rd and 26th week, thereafter decreasing gradually, reaching a value of 108 ng/ml at birth. pTM continues to decrease progressively during childhood, reaching in the 5-15 years group a median of 56 ng/ml which approaches the adult value. The pTM peak was statistically significant and represents a specific foetal phenomenon as it was independent of the corresponding maternal values. As a whole, the pTM pattern during foetal maturation appears totally different from that of protein C, prothrombin and other coagulation activators and inhibitors and thus, TM may play in the foetus another role in addition to its well-known anticoagulant function.

APC Resistance and other Haemostatic Variables during Pregnancy and Puerperium

1999 ◽  
Vol 81 (04) ◽  
pp. 527-531 ◽  
Author(s):  
U. Kjellberg ◽  
N.-E. Andersson ◽  
S. Rosén ◽  
L. Tengborn ◽  
M. Hellgren
Keyword(s):  
Factor Viii ◽  
Plasminogen Activator ◽  
Protein C ◽  
Activated Protein C ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Reference Level ◽  
Soluble Fibrin ◽  
Prothrombin Fragment ◽  
D Dimer

SummaryForty-eight healthy pregnant women were studied prospectively and longitudinally. Blood sampling was performed at 10-15, 23-25, 32-34 and 38-40 weeks of gestation, within one week and at eight weeks postpartum. Classic and modified activated protein C ratio decreased as pregnancy progressed. In the third trimester 92% of the ratios measured with the classic test were above the lower reference level whereas all modified test ratios were normal. Slight activation of blood coagulation was shown with increased levels of prothrombin fragment 1+2, soluble fibrin and D-dimer. Fibrinogen, factor VIII and plasminogen activator inhibitor type 1 and type 2 increased. Protein S and tissue plasminogen activator activity decreased. Protein C remained unchanged. No correlation was found between the decrease in classic APC ratio and changes in factor VIII, fibrinogen, protein S, prothrombin fragment 1+2 or soluble fibrin, nor between the increase in soluble fibrin and changes in prothrombin fragment 1+2, fibrinogen and D-dimer.

Beckenvenenthrombose im 16. Lebensjahr bei angeborener Vena-cava-inferior-Atresie und Ecstasy-Abusus

Phlebologie ◽  
2003 ◽  
Vol 32 (02) ◽  
pp. 50-53
Author(s):  
C. Pieck ◽  
P. Sander ◽  
F. G. Bechara ◽  
P. Altmeyer ◽  
M. Stücker
Keyword(s):  
Protein C ◽  
Vena Cava ◽  
Protein S ◽  
Sich Eine ◽  
Farbkodierte Duplexsonographie ◽  
Vena Cava Inferior ◽  
Vena Iliaca ◽  
Vena Femoralis

ZusammenfassungKasuistik: Eine kaukasische Patientin, die sich wegen kosmetisch störender Varizen an der Bauchdecke und den Leisten vorstellte, erlitt mit 16 Jahren während einer exzessiven Tanzveranstaltung unter dem Einfluss von Ecstasy (3,4-Methylendioxymethamphetamin) aus kompletter Gesundheit bei damals asymptomatischer Vena-cava-inferior-Atresie eine akute Beckenvenenthrombose. Diagnostik: Bidirektionale Dopplersonographie, farbkodierte Duplexsonographie, Kernspintomographie mit Magnevist-Kontrastmittel der Venen beider Beine bzw. im Bereich des kleinen Beckens, Bestimmung der Serumkonzentration von Protein C und Protein S, Ausschluss von APC-Resistenz und Faktor-V-Leiden-Mutation. Ergebnisse: In der farbkodierten Duplexsonographie thrombosierte Vena iliaca externa sowie septierte, jedoch suffiziente Vena femoralis communis beidseits, keine Insuffizienzen oder Thromben in den übrigen extraund intrafaszialen Beinvenen nachweisbar. In der Kernspintomographie der Beckenvenen stellte sich eine Hypoplasie der Vena cava inferior oberhalb der Nierenetage und eine Atresie der Vena cava inferior unterhalb der Nierenetage dar sowie ein ausgeprägter venöser Kollateralkreislauf im Bereich des Beckens über die Vv. iliacae internae beidseits und die Vv. lumbales ascendentes beidseits bei varikös entarteten Kollateralvenen im Bereich der Bauchdecke beidseits mit Anschluss an die V. femoralis communis beidseits. Die untersuchten Gerinnungsparameter blieben unauffällig. Schlussfolgerung: Ecstasy-Abusus kann in Kombination mit starker körperlicher Anstrengung zu Exsikkose und Hämokonzetration führen. Dies sehen wir als letzte Ursache der Thrombose bei bestehender Vena-cava-Aplasie.

Gerinnungsstörungen und Schlaganfall

2006 ◽  
Vol 26 (04) ◽  
pp. 309-315 ◽  
Author(s):  
Ch. C. Eschenfelder ◽  
R. Stingele ◽  
J. A. Zeller
Keyword(s):  
Protein C ◽  
Foramen Ovale ◽  
Offenes Foramen Ovale ◽  
At Iii

ZusammenfassungHereditäre und erworbene Gerinnungsstörungen können bei der Schlaganfallentstehung eine wichtige Rolle spielen. Wegen der Seltenheit der meisten erblichen Gerinnungsstörungen und der erheblichen Kosten, die sich aus einer unkritischen Indikationsstellung ergeben, ist eine maßgeschneiderte Diagnostik sinnvoll. Suggestive Hinweise auf eine Gerinnungsstörung sind niedriges Lebensalter, mehrfache Thrombosen in der Anamnese, altersuntypische Gefäßdegenerationen, vorherige Aborte bei Schlaganfallpatientinnen oder strukturelle Herzveränderungen (z. B. offenes Foramen ovale). Störungen von AT III, Protein C und S, APC-Resistenz, Prothrombinmutation, Homocysteinämie, Antiphospholipidantikörper und prokoagulatorische zelluläre Interaktionen werden diskuiert.

Dermatan Sulfate and LMW Heparin Enhance the Anticoagulant Action of Activated Protein C

1999 ◽  
Vol 82 (11) ◽  
pp. 1462-1468 ◽  
Author(s):  
José Fernández ◽  
Jari Petäjä ◽  
John Griffin
Keyword(s):  
Molecular Weight ◽  
Unfractionated Heparin ◽  
Protein C ◽  
Dermatan Sulfate ◽  
Anticoagulant Activity ◽  
Activated Protein C ◽  
Factor V ◽  
Factor Va ◽  
Anticoagulant Action

SummaryUnfractionated heparin potentiates the anticoagulant action of activated protein C (APC) through several mechanisms, including the recently described enhancement of proteolytic inactivation of factor V. Possible anticoagulant synergism between APC and physiologic glycosaminoglycans, pharmacologic low molecular weight heparins (LMWHs), and other heparin derivatives was studied. Dermatan sulfate showed potent APC-enhancing effect. Commercial LMWHs showed differing abilities to promote APC activity, and the molecular weight of LMWHs correlated with enhancement of APC activity. Degree of sulfation of the glycosaminoglycans influenced APC enhancement. However, because dextran sulfates did not potentiate APC action, the presence of sulfate groups per se on a polysaccharide is not sufficient for APC enhancement. As previously for unfractionated heparin, APC anticoagulant activity was enhanced by glycosaminoglycans when factor V but not factor Va was the substrate. Thus, dermatan sulfate and LMWHs exhibit APC enhancing activity in vitro that could be of physiologic and pharmacologic significance.

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