Anticoagulant Properties of the Vascular Endothelium

Bombeli, Thomas; Mueller, Michele; Haeberli, André

doi:10.1055/s-0038-1655981

Cited by 211 publications

(103 citation statements)

References 291 publications

(217 reference statements)

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“…This newly detected, meaningful location allows them, in stark contrast with the pericytes, to activate protein C rapidly and to counteract subendothelially induced coagulation processes promptly within their junctions (26). This agrees well with the expanded knowledge about the central antithrombogenic roles of vascular endothelium, not only through the expression of various anticoagulatory (coagulation inhibiting) but also of antiaggregatory (platelet inhibiting) and profibrinolytic (fibrinolysis promoting) activities (7,64,69,70).…”

Section: Discussionsupporting

confidence: 81%

Pericytes in the macrovascular intima: possible physiological and pathogenetic impact

Juchem¹,

Weiss

Gansera

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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The frequently observed de-endothelialization of venous coronary bypass grafts prepared using standard methods exposes subendothelial prothrombotic cells to blood components, thus endangering patients by inducing acute thromboembolic infarction or long-term proliferative stenosis. Our aim was to gain deeper histological and physiological insight into these relations. An intricate network of subendothelial cells, characterized by histological features specific for true pericytes, was detected even in healthy vessels and forms, coupled to the luminal endothelium, a second leaflet of the macrovascular intima. These cells, and particularly those in the venous intima, express enormous concentrations of tissue factor and can recruit additional amounts of up to the 25-fold concentration within 1 h during preincubation with serum (intimal pericytes of venous origin activate 30.71 ± 4.07 pmol coagulation factor x·min−1·10−6 cells; n = 15). Moreover, decoupled from the endothelium, they proliferate rapidly (generation time, 15 ± 2.1 h, n = 8). Central regions of atherosclerotic plaques, as well as of those of restenosed areas of coronary vein grafts, consist almost completely of these cells. In stark contrast with the prothrombogenicity of the intimal pericytes, intact luminal endothelium recruits high concentrations of thrombomodulin (CD 141) specifically within its intercellular junctions, activates Protein C rapidly (42 ± 5.1 pmol/min·106 venous endothelial cells at thrombin saturation; n = 15), can thus actively prevent coagulatory processes, and never expresses histologically detectable and functionally active tissue factor. Given this strongly prothrombotic potential of the intimal pericytes and their overshooting growth behavior in endothelium-denuded vascular regions, they may play important roles in the development of atherosclerosis, thrombosis, and saphenous vein graft disease.

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Section: Discussionsupporting

confidence: 81%

Pericytes in the macrovascular intima: possible physiological and pathogenetic impact

Juchem¹,

Weiss

Gansera

et al. 2010

American Journal of Physiology-Heart and Circulatory Physiology

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“…Interestingly, another measure of procoagulant activity, increased TF surface expression, was induced only in cells infected with ASFV. The coagulation process is initiated by exposure of TF on the cell surface, which then activates factor VII (8,26). TF is rapidly synthesized after endothelial cell activation through NF-B-dependent and independent pathways.…”

Section: Discussionmentioning

confidence: 99%

African Swine Fever Virus Infection of Porcine Aortic Endothelial Cells Leads to Inhibition of Inflammatory Responses, Activation of the Thrombotic State, and Apoptosis

Vallée

Tait

Powell

2001

J Virol

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“…22,69 Endothelial dysfunction may, hence, contribute to the thrombotic process, a feature of most forms of PH. A relative deficiency of the antithrombotic molecules prostacyclin and NO (see above) and slowing of blood flow in the pulmonary circulation secondary to luminal narrowing further enhances thromogenicity.…”

Section: Endothelial Dysfunction and Hypercoagulabilitymentioning

confidence: 99%