Long-Term Effect of 17β-Estradiol and Thrombin on Tissue Factor Pathway Inhibitor Release from HUVEC☆

Bilsel, A Serpil; Onaran, Nurperi; Moini, Hadi; Emerk, Kaya

doi:10.1016/s0049-3848(00)00228-0

Cited by 20 publications

(14 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…It appears that while EE or NETA effects on plasma lipoproteins may contribute to changes in plasma TFPI, other mechanisms are probably at work also. It has been previously reported that treatment of cultured human umbilical vein endothelial cells (HUVEC) with17␤-estradiol reduced TFPI release [57]. We were unable to reproduce those observations nor see a NETA effect on TFPI release by HU-VEC in our laboratory, perhaps because the HUVEC used in our studies lacked detectable ER (data not shown).…”

Section: Discussionmentioning

confidence: 58%

Differential effects of estrogens and progestins on the anticoagulant tissue factor pathway inhibitor in the rat

Shirk¹,

Zhang²,

Winneker³

2005

The Journal of Steroid Biochemistry and Molecular Biology

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 58%

Differential effects of estrogens and progestins on the anticoagulant tissue factor pathway inhibitor in the rat

Shirk¹,

Zhang²,

Winneker³

2005

The Journal of Steroid Biochemistry and Molecular Biology

View full text Add to dashboard Cite

“…Of interest, thrombin has an inhibitory effect on the production of TFPI by endothelial cells[91], and the increased thrombin generation observed in patients with PTL may be associated with a concomitant reduction in TFPI production by the maternal vascular endothelium. The placenta is an additional source for TFPI (mainly TFPI-2[92–101]), and preterm parturition may be associated with a lower production of TFPI by the placenta, contributing to the low maternal plasma concentrations detected in patients with PTL.…”

Section: Discussionmentioning

confidence: 99%

High tissue factor activity and low tissue factor pathway inhibitor concentrations in patients with preterm labor

Erez

Romero²,

Vaisbuch

et al. 2009

The Journal of Maternal-Fetal & Neonatal Medicine

View full text Add to dashboard Cite

Objective Preterm labor (PTL) has been associated with an increased thrombin generation in the maternal circulation and amniotic fluid. Tissue factor (TF) is a potent initiator of the coagulation cascade, which can trigger the hemostatic system to generate thrombin. The aims of this study were to determine whether spontaneous PTL with intact membranes is associated with changes in the maternal plasma concentrations and activity of TF and tissue factor pathway inhibitor (TFPI). Methods This cross-sectional study included women in the following groups: 1) normal pregnancies (n=86); 2) term pregnancies in spontaneous labor (TIL) (n=67) and not in labor (TNL) (n=88); and 3) patients with spontaneous PTL and intact membranes (n=136) that were classified into three sub-groups: a) PTL without intra-amniotic infection and/or inflammation (IAI) who delivered at term (n=49), b) PTL without IAI who delivered preterm (n=54), and c) PTL with IAI who delivered preterm (n=33). Plasma concentrations of TF and TFPI were measured by ELISA, and their activity was measured by chromogenic assays. Non-parametric statistics were used for analysis. Results 1) Among women at term, those with spontaneous labor had a higher median maternal plasma TF and a lower median TFPI concentrations than that of those without labor. 2) Patients with PTL had a significantly lower median maternal plasma TFPI concentration than that of normal pregnant women, regardless of the presence of IAI. 3) There was no significant differences in the median maternal plasma TF concentrations between patients with a normal pregnancy and those with PTL. 4) In contrast, the median TF activity was higher among patients with PTL than in women with normal pregnancies, regardless of the presence of IAI or preterm delivery. 5) However, maternal plasma TFPI activity did not differ among the study groups. Conclusion Women with preterm parturition, in contrast to those in labor at term, have a higher TF activity and a lower TFPI concentration, without a significant change in the median maternal plasma TF concentration. These observations suggest that the increased thrombin generation reported in patients with PTL may be the result of activation of the extrinsic pathway of the coagulation cascade. In addition, the increased thrombin generation reported in patients with PTL could be due to insufficient anti-coagulation, as reflected by the low maternal plasma TFPI concentration.

show abstract

“…Estrogen treatment reduces TFPI secretion from cultured endothelial cells, and oral contraceptive use and estrogen treatment reduce plasma circulating TFPI antigen and activity in women (5,18,37). However, it is not known whether Fig.…”

Section: Discussionmentioning

confidence: 99%

Estrogenic regulation of tissue factor and tissue factor pathway inhibitor in platelets

Jayachandran

Sanzo

Owen

et al. 2005

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

Oral estrogen treatment increases thrombotic risk. Tissue factor (TF), tissue factor pathway inhibitor (TFPI), and platelet interaction with leukocytes are important determinants of thrombogenesis. Therefore, the present study was designed to define and compare platelet TF and TFPI mRNA and adhesion protein expression in platelets derived from animals treated with different types of oral estrogens. Ovariectomized pigs were treated with 17beta-estradiol (2 mg/day), conjugated equine estrogen (CEE; 0.625 mg/day), or raloxifene (60 mg/day) for 4 wk. Compared with intact animals, ovariectomy and treatment differentially affected populations of leukocytes: neutrophils decreased whereas lymphocytes increased significantly 4 wk after ovariectomy and with 17beta-estradiol and CEE treatments; eosinophils increased only with 17beta-estradiol treatment. Content of TF protein increased in platelets from 17beta-estradiol- and raloxifene-treated pigs, whereas TF mRNA was detected only in platelets from 17beta-estradiol- and CEE treated pigs. TFPI mRNA increased in platelets after ovariectomy and estrogen treatment. Only a trace of TFPI protein was detected, but a higher-molecular-mass protein was observed in all treatment groups. Expression of CD40 and CD40 ligand increased with ovariectomy and decreased with 17beta-estradiol and CEE treatments more than with raloxifene. The ratio of activated to basal P-selectin expression decreased with ovariectomy and increased with raloxifene treatments. These results suggest that estrogenic formulations may affect individual thrombotic risk by different mechanisms that regulate TF and platelet-leukocytic interactions. These studies provide the rationale for evaluation of interactions among platelets and TF and TFPI expression on thrombin generation during estrogen treatment in humans.

show abstract

Long-Term Effect of 17β-Estradiol and Thrombin on Tissue Factor Pathway Inhibitor Release from HUVEC☆

Cited by 20 publications

References 29 publications

Differential effects of estrogens and progestins on the anticoagulant tissue factor pathway inhibitor in the rat

Differential effects of estrogens and progestins on the anticoagulant tissue factor pathway inhibitor in the rat

High tissue factor activity and low tissue factor pathway inhibitor concentrations in patients with preterm labor

Estrogenic regulation of tissue factor and tissue factor pathway inhibitor in platelets

Contact Info

Product

Resources

About