Changes of plasma and placental tissue factor pathway inhibitor-2 in women with preeclampsia and normal pregnancy

Xiong, Yan; Zhou, Qiongjie; Jiang, Fanglin; Zhou, Shu‐Feng; Lou, Yiting; Guo, Qisang; Wang, Liang; Kong, Desheng; Ma, Ding; Li, Xiaotian

doi:10.1016/j.thromres.2010.02.017

Cited by 22 publications

(39 citation statements)

References 36 publications

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“…In agreement with recent observations (36,38), our data indicate that plasma levels of TFPI-2 in pregnancy during the onset of labor are ϳ7 nM. Based upon previous work with TFPI-1 (46, 47, 54 -56), we evaluated the binding of TFPI-2 to purified FV and FVa as well as to FV/Va in platelets and FV in pregnant woman plasma.…”

Section: Discussionsupporting

confidence: 87%

“…The plasma TFPI-2 levels in the third trimester of pregnancy range from the early reports of 1-3 nM (31)(32)(33)(34)(35) to up to 10 nM in recent reports (36,38). In one study, the mean plasma TFPI-2 level in pregnancy is reported to be 320 pM (31).…”

mentioning

confidence: 97%

“…Human plasma TFPI-2 levels are reported to be negligible (6,(31)(32)(33)(34)(35)(36); however, a mean value of 30 pM (range from 3 to 300 pM) in one study (37) and an average value of 0.5 nM (range not given) in an another study (38) have also been reported. Thus, plasma levels of TFPI-2 are below the limit of detection (Յ20 pM or 0.5 ng/ml) in the majority of the reports and are also observed to be low in the TFPI-2-transfected apoE-knock-out mice (39).…”

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confidence: 99%

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Platelets Contain Tissue Factor Pathway Inhibitor-2 Derived from Megakaryocytes and Inhibits Fibrinolysis

Vadivel

Ponnuraj

Kumar

et al. 2014

Journal of Biological Chemistry

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Background: TFPI-2 inhibits plasma kallikrein, FXIa, and plasmin, but its concentration in normal plasma is insufficient to inhibit clotting or fibrinolysis. Results: Platelets contain TFPI-2 derived from megakaryocytes and binds to platelet FV/Va and circulating FV in late pregnancy when plasma TFPI-2 is ϳ7 nM. Conclusion: Platelet-derived TFPI-2 regulates intrinsic coagulation and tPA-induced fibrinolysis. Significance: Platelet-derived TFPI-2 promotes clot stabilization while attenuating intrinsic clotting.

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Section: Discussionsupporting

confidence: 87%

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confidence: 97%

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confidence: 99%

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Platelets Contain Tissue Factor Pathway Inhibitor-2 Derived from Megakaryocytes and Inhibits Fibrinolysis

Vadivel

Ponnuraj

Kumar

et al. 2014

Journal of Biological Chemistry

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“…TFPI-2 has also been associated with coagulation and fibrinolysis regulation (Zawadzki et al 2009). TFPI-2 interferes with the tissue factor (TF) pathway through inhibition of the TF-factor VIIa complex and reduced expression has been linked to many pathophysiological processes, including atherosclerosis and tumor growth (Zhang et al 2012),(Xiong et al 2010). Lower maternal plasma levels of TFPI-2 have been associated with preeclampsia (Matsuoka et al 1997; Hafner et al 2004).…”

Section: Discussionmentioning

confidence: 99%

Pregnancy complicated by obesity induces global transcript expression alterations in visceral and subcutaneous fat

et al. 2014

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Maternal obesity is a significant risk factor for development of both maternal and fetal metabolic complications. Increase in visceral fat and insulin resistance is a metabolic hallmark of pregnancy, yet little is known how obesity alters adipose cellular function and how this may contribute to pregnancy morbidities. We sought to identify alterations in genome-wide transcription expression in both visceral (omental) and abdominal subcutaneous fat deposits in pregnancy complicated by obesity. Visceral and abdominal subcutaneous fat deposits were collected from normal weight and obese pregnant women (n=4/group) at time of scheduled uncomplicated cesarean section. A genome-wide expression array (Affymetrix Human Exon 1.0 st platform), validated by quantitative real-time PCR, was utilized to establish the gene transcript expression profile in both visceral and abdominal subcutaneous fat in normal weight and obese pregnant women. Global alteration in gene expression was identified in pregnancy complicated by obesity. These regions of variations lead to identification of indolethylamine N-methyltransferase (INMT), tissue factor pathway inhibitor-2 (TFPI-2), and ephrin type-B receptor 6 (EPHB6), not previously associated with fat metabolism during pregnancy. In addition, subcutaneous fat of obese pregnant women demonstrated increased coding protein transcripts associated with apoptosis compared to lean counterparts. Global alteration of gene expression in adipose tissue may contribute to adverse pregnancy outcomes associated with obesity.

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“…A possible explanation of the lower maternal plasma concentration observed in some of the obstetrical syndromes may be that during these syndromes there is a reduction in the placental production of TFPI 65,66,69,76 (mainly TFPI-2), contributing to the low maternal plasma concentrations detected in patients with PTL, in addition to the thrombin inhibitory effect to TFPI expression on endothelial cells, as above mentioned. Indeed, patients with vascular complications of pregnancy (preeclampsia, eclampsia, placental abruption, fetal growth restriction, and fetal demise) have a lower placental concentration of total TFPI, and TFPI mRNA expression than in women with normal pregnancies 78,79 . Other proteins implicated in the inhibitory control of the coagulation cascade are protein S, protein C and protein Z.…”

Section: Depleted or Insufficient Anticoagulant Proteins Concentrationmentioning

confidence: 99%

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

Mastrolia

Mazor

Loverro

et al. 2014

Preprint

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View the peer-reviewed version (peerj.com/articles/653), which is the preferred citable publication unless you specifically need to cite this preprint. Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromesObstetrical complications including preeclampsia, fetal growth restriction, preterm labor, preterm prelabor rupture of membranes and fetal demise are all the clinical endpoint of several underlying mechanisms (i.e. infection inflammation, thrombosis, endocrine disorder, immunologic rejection, genetic, and environmental), therefore, they may be regarded as syndromes. Placental vascular pathology and increased thrombin generation were reported in all of these obstetrical syndromes. Moreover, elevated concentrations of thrombin-antithrombin III complexes and changes in the coagulation as well as anticoagulation factors can be detected in the maternal circulation prior to the clinical development of the disease in some of these syndromes. In this review, we will assess the changes in the hemostatic system during normal and complicated pregnancy in maternal blood, maternal-fetal interface and amniotic fluid, and describe the contribution of thrombosis and vascular pathology to the development of the great obstetrical syndromes.PeerJ PrePrints | http://dx.doi.org/10.7287/peerj.preprints.487v1 | CC-BY 4.0 Open Access |

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Changes of plasma and placental tissue factor pathway inhibitor-2 in women with preeclampsia and normal pregnancy

Cited by 22 publications

References 36 publications

Platelets Contain Tissue Factor Pathway Inhibitor-2 Derived from Megakaryocytes and Inhibits Fibrinolysis

Platelets Contain Tissue Factor Pathway Inhibitor-2 Derived from Megakaryocytes and Inhibits Fibrinolysis

Pregnancy complicated by obesity induces global transcript expression alterations in visceral and subcutaneous fat

Placental vascular pathology and increased thrombin generation as mechanisms of disease in obstetrical syndromes

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