Tumor necrosis factor/cachectin-induced modulation of endothelial cell hemostatic properties

P. P. Nawroth, David Stern

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Tumor necrosis factor/cachectin (TNF) is a mediator of the septic shock state, which can modulate hemostatic properties of the vessel wall. The interaction of TNF with endothelium is not cytotoxic, rather it is receptor mediated and results in a change in receptor expression on the endothelial cell surface, enabling endothelium to actively promote coagulation. Anticoagulant mechanisms, including the protein C/protein S system and fibrinolysis are suppressed, whereas the initiation and propagation of procoagulant activity is enhanced. This unidirectional shift in vessel wall coagulant activity favoring clot formation could contribute to the coagulopathy associated with sepsis and indicates a mechanism through which the coagulation system serves as an integral part of the host response.

Original languageEnglish (US)
Pages (from-to)254-258
Number of pages5
JournalOncology Research and Treatment
Volume10
Issue number4
DOIs
StatePublished - Jan 1 1987
Externally publishedYes

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Hemostatics
Endothelium
Endothelial Cells
Tumor Necrosis Factor-alpha
Coagulants
Protein S
Fibrinolysis
Septic Shock
Protein C
Anticoagulants
Sepsis

All Science Journal Classification (ASJC) codes

  • Cancer Research
  • Hematology
  • Oncology

Cite this

Tumor necrosis factor/cachectin-induced modulation of endothelial cell hemostatic properties. / Nawroth, P. P.; Stern, David.

In: Oncology Research and Treatment, Vol. 10, No. 4, 01.01.1987, p. 254-258.

Research output: Contribution to journalArticle

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