Elevated levels of leukocyte tissue factor mRNA in patients with venous thromboembolism

Kamikura, Yuko; Wada, Hideo; Kobayashi, Toshihiko; Sase, Tomohiro; Nishikawa, Masakatsu; Ishikura, Ken; Yamada, Norikazu; Abe, Yasunori; Nishioka, Junji; Nakano, Takeshi; Shiku, Hiroshi

doi:10.1016/j.thromres.2004.12.013

Cited by 24 publications

(16 citation statements)

References 24 publications

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“…It has been reported that TF levels were significantly elevated during VTE [24] or arterial thrombotic disease, including CHD [25]. TF levels seem to be increased in thrombotic conditions, as we observed a similar trend.…”

Section: Discussionsupporting

confidence: 87%

Genetic polymorphisms and plasma levels of tissue factor and tissue factor pathway inhibitor in venous thromboembolism

Kwon¹,

Jo³

et al. 2014

Blood Coagulation &Amp; Fibrinolysis

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Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) play important roles in coagulation. The aim of this study was to investigate the distributions of TF and TFPI polymorphisms in Koreans and to analyze the association of these genetic polymorphisms with plasma levels and development of venous thromboembolism (VTE). The polymorphisms TF 5466 A > G, TF -603 A > G, TFPI -287 T > C and TFPI -33 T > C were investigated in 40 Korean VTE patients and 40 age-matched and sex-matched controls by real-time PCR followed by melting curve analysis and DNA sequence analysis. Plasma levels of TF and TFPI were measured by enzyme-linked immunosorbent assay. The G allele of TF 5466 was not detected, and allelic frequencies of TF -603 G, TFPI -287 C and TFPI -33 C were 27.5, 67.5 and 16.2%, respectively. The distributions of TF and TFPI polymorphisms were not different between patients and controls. The presence of TF -603 G allele was correlated with low plasma TF levels (P = 0.029). Mean plasma TFPI levels were similar between TFPI genotypic groups. Although not statistically significant, plasma TF and TFPI levels were higher in patients than controls. The distributions of TF and TFPI polymorphisms in Koreans were considerably different from whites, suggesting ethnic variations. The TF -603 A > G polymorphism was significantly correlated with decreased plasma TF levels. Neither genetic polymorphisms in TF and TFPI nor their plasma levels seem to act as direct risk factors for VTE.

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Section: Discussionsupporting

confidence: 87%

Genetic polymorphisms and plasma levels of tissue factor and tissue factor pathway inhibitor in venous thromboembolism

Kwon¹,

Jo³

et al. 2014

Blood Coagulation &Amp; Fibrinolysis

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“…It has been reported that miR‐146a/b downregulates the senescence through the inhibition of the secretion of inflammatory cytokines IL‐6 and IL‐8 . The mRNA level of TF in leukocytes is higher in patients with DVT than that in healthy individuals . As an integral component of the fibrinolytic system, PAI‐1 has been suggested to play a regulatory role in venous thrombosis resolution .…”

Section: Discussionmentioning

confidence: 99%

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

et al. 2019

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Studies have shown that microRNAs (miRNAs) participate in almost all pathological and physiological processes including acute lower‐extremity deep venous thrombosis (LEDVT). Here, this study was designed to elucidate the possible function of miR‐103a‐3p in acute LEDVT. Expression of miR‐103a‐3p and chemokine C‐X‐C motif ligand 12 (CXCL12) was initially quantified in plasma collected from 81 LEDVT patients. Then LEDVT mouse models were established by injection with 3% sodium pentobarbital. The interaction between miR‐103a‐3p and CXCL12 was identified by dual‐luciferase reporter gene assay. After gain‐ and loss‐of‐function studies, interleukin‐6 (IL‐6) and IL‐8 and tissue factor (TF) levels, and expression of plasminogen activator inhibitors (PAIs), von Willebrand factor (vWF), thromboxane A2 (TH‐A2), F4/80, IL‐12, Arginase‐1 (Arg‐1) and CD206 were determined using enzyme‐linked immunosorbent assay (ELISA), reverse transcription quantitative polymerase chain reaction (RT‐qPCR) and western blot analysis, respectively. miR‐103a‐3p was downregulated, while CXCL12 was upregulated in patients and mice with LEDVT. miR‐103a‐3p targets CXCL12 and inhibited its expression. Overexpressed miR‐103a‐3p or downregulated CXCL12 decreased expression of IL‐6, IL‐8, TF, PAIs, vWF, TH‐A2, M1 markers (IL‐6 and IL‐12), yet increased expression of M2 markers (Arg‐1 and CD206) in LEDVT mice. Additionally, upregulated miR‐103a‐3p or silencing CXCL12 suppressed thrombosis in LEDVT mice. However, overexpression of CXCL12 reversed the tendency mentioned above. Altogether, miR‐103a‐3p can potentially downregulate CXCL12 expression to disrupt inflammatory response and thrombosis, ultimately preventing the development of LEDVT. Our findings underscore a possible alternative therapeutic strategy to limit LEDVT.

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“…TF plays a role in venous thrombosis as well [18], and this is particularly relevant in the context of the high prevalence of pulmonary embolism in COPD patients [4]. Elevated leukocyte TF mRNA has been observed in patients with venous thromboembolism [19], and reduced plasma TF levels (due to TF gene polymorphisms) are associated with lower risk of venous thrombosis [20]. …”

Section: Discussionmentioning

confidence: 99%

Circulating tissue factor procoagulant activity is elevated in stable moderate to severe chronic obstructive pulmonary disease

Vaidyula

Criner

Grabianowski

et al. 2009

Thrombosis Research

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Elevated levels of leukocyte tissue factor mRNA in patients with venous thromboembolism

Cited by 24 publications

References 24 publications

Genetic polymorphisms and plasma levels of tissue factor and tissue factor pathway inhibitor in venous thromboembolism

Genetic polymorphisms and plasma levels of tissue factor and tissue factor pathway inhibitor in venous thromboembolism

Overexpressed microRNA‐103a‐3p inhibits acute lower‐extremity deep venous thrombosis via inhibition of CXCL12

Circulating tissue factor procoagulant activity is elevated in stable moderate to severe chronic obstructive pulmonary disease

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