IndraLab

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TNF increases the amount of THBD. 21 / 23
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"Beraprost, prostacyclin and db-cAMP also effectively blocked the interleukin-1- and tumor necrosis factor induced depression of TM expression substantially."

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"The preadministration of hemin to septic mice increased the expression and activity of HO-1; inhibited thrombosis in the preceding 3 organs; prolonged PT and APTT; inhibited the production of TNF-alpha and IL-6; upregulated the expression of PC and TM in livers; elevated the plasma levels of PCand aPC; and reduced the plasma levels of TM."

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"In vitro, tumor necrosis factor (TNF) induces endothelial expression of the procoagulant, tissue factor, and downregulation of thrombomodulin, a key component of the thrombomodulin and protein C (PC)/protein S (PS) pathway, which normally maintains an anticoagulant state by inactivating thrombin, preventing further thrombin formation by degrading factors Va and VIIIa, and decreasing plasminogen activator inhibitor activity."

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"TM is expressed constitutively on endothelium and it has been previously demonstrated that both TNF-a and IL-1a and b cause a slow loss of TM and endothelial cell protein C receptor from the surface of endothelial cells [XREF_BIBR]."

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"TNFalpha and IL-1beta promote thrombosis at the vascular wall by inducing endothelial expression of tissue factor and downregulating expression of thrombomodulin, the endothelial thrombin receptor that plays a key role in the activation of the anticoagulant protein C pathway."

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"It is possible that molecules such as endotoxin, interleukin-1, and tumor necrosis factor are able to modulate the expression of TM in these cells [19]."

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"The concerted action of TNF-α and neutrophils promotes TM release from the endothelial cells."

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"Suppression of endothelial thrombomodulin expression by TNF-alpha has been documented [XREF_BIBR]."

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"TNF-mediated stimulation of hAECs increased not only TF-antigen, TF-activity and PS-exposure, but also TFPI and thrombomodulin expression."

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"Recently, it has been shown that JNK and p38 mediated TNFα induced down-regulation of TM expression [42] ."

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"Unlike IKKbeta knockdown cells, TNFalpha treatment significantly reduced (P < 0.0001) TM protein expression in IKKbeta KD/SSEE cells compared with untreated IKKbeta KD/SSEE cells (XREF_FIG)."

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"In tissue culture, TNF, IL-1 or endotoxin lead to a slow loss of TM and endothelial cell Protein C receptor (EPCR) from the cell surface."

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"A major component of this response is a reduction in expression of thrombomodulin, a cell surface cofactor for the activation of protein C. Regulation of thrombomodulin expression by TNF has been reported to occur through multiple mechanisms."

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"Although tumour necrosis factor-a (TNF-a) and interleukin-1ß (IL-1ß) have been found to up-regulate macrophage expression of TM, these cytokines suppress thrombomodulin expression in endothelial cells[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Endothelial cell culture and animal studies have indicated that TNF-alpha and IL-1 enhance the pro coagulant response by down regulating expression of thrombomodulin and protein C synthesis [XREF_BIBR, XREF_BIBR]."

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"To assess whether the expression of TM is influenced by freezing/thawing process, we evaluated the basal and TNF-induced cell surface expression of TM on expanded HUVEC."

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"To assess whether the expression of TM is influenced by freezing/thawing process, we evaluated the basal and TNF-induced cell surface expression of TM on expanded HUVEC."

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"TNFα also induces catabolic processes in synovial joint and directly regulates intra-articular levels of FVIIIa modulating expression of thrombomodulin (TM) (Aggarwal et al., 2012; Wojdasiewicz et al., 2018)."

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"To assess whether the expression of TM is influenced by freezing/thawing process, we evaluated the basal and TNF-induced cell surface expression of TM on expanded HUVEC."

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"TNF and IL-1 promote blood coagulation by inhibiting the expression of thromboregulatory protein (TM) and reducing the production of activated protein C (APC), thus promoting the coagulation reaction [61,62]."

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"These proinflammatory cytokines further drive excess endothelial cell TF expression, and TNF-α also decreases thrombomodulin transcription, leading to hypercoagulability and impaired regulation of coagulation [94,95,96,97,98]."