ArticleBlood2008
Maternal Par4 and platelets contribute to defective placenta formation in mouse embryos lacking thrombomodulin.
Article in Blood, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
13 citing papers in PubMed, 43 citations in OpenAlex.
- Platelets link coagulation and complement in regulating murine placental vascular development.The Journal of clinical investigation · 2026Article
- Intercellular synergy between protease-activated receptors 1 and 4 during mouse development.Journal of thrombosis and haemostasis : JTH · 2025Article
- Exploring the Role of Platelets in Virus-Induced Inflammatory Demyelinating Disease and Myocarditis.International journal of molecular sciences · 2024Article
- Changes of new coagulation markers in healthy pregnant women and establishment of reference intervals in Changsha.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2022Article
- Combined thrombogenic effects of vessel injury, pregnancy and procoagulant immune globulin administration in mice.Thrombosis journal · 2020Article
- Expression of Pinopodes in the Endometrium from Recurrent Pregnancy Loss Women. Role of Thrombomodulin and Ezrin.Journal of clinical medicine · 2020Article
- Hydroxychloroquine may be beneficial in preeclampsia and recurrent miscarriage.British journal of clinical pharmacology · 2020Review
- Maternal Platelets—Friend or Foe of the Human Placenta?International journal of molecular sciences · 2019Review
- Candidate SNP markers of reproductive potential are predicted by a significant change in the affinity of TATA-binding protein for human gene promoters.BMC genomics · 2018Article
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- The protein C pathway in tissue inflammation and injury: pathogenic role and therapeutic implications.Blood · 2010Review
- Placental thrombomodulin expression in recurrent miscarriage.Reproductive biology and endocrinology : RB&E · 2010Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Absence of the blood coagulation inhibitor thrombomodulin (Thbd) from trophoblast cells of the mouse placenta causes a fatal arrest of placental morphogenesis. The pathogenesis of placental failure requires tissue factor, yet is not associated with increased thrombosis and persists in the absence of fibrinogen. Here, we examine the role of alternative targets of coagulation that might contribute to the placental failure and death of Thbd(-/-) embryos. We demonstrate that genetic deficiency of the protease-activated receptors, Par1 or Par2, in the embryo and trophoblast cells does not prevent the death of Thbd(-/-) embryos. Similarly, genetic ablation of the complement pathway or of maternal immune cell function does not decrease fetal loss. In contrast, Par4 deficiency of the mother, or the absence of maternal platelets, restores normal development in one-third of Thbd-null embryos. This finding generates new evidence implicating increased procoagulant activity and thrombin generation in the demise of thrombomodulin-null embryos, and suggests that platelets play a more prominent role in placental malfunction associated with the absence of thrombomodulin than fibrin formation. Our findings demonstrate that fetal prothrombotic mutations can cause localized activation of maternal platelets at the feto-maternal interface in a mother with normal hemostatic function.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.