ArticleBlood2021
Heightened activation of embryonic megakaryocytes causes aneurysms in the developing brain of mice lacking podoplanin.
Article in Blood, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- A subset of megakaryocytes regulates development of hematopoietic stem cell precursors.The EMBO journal · 2024Article
- Novel GNE missense variants impair de novo sialylation and cause defective angiogenesis in the developing brain in mice.Blood advances · 2024Article
- Immunothrombosis versus thrombo-inflammation: platelets in cerebrovascular complications.Research and practice in thrombosis and haemostasis · 2024Article
- C-type lectin-like receptor 2 specifies a functionally distinct subpopulation within phenotypically defined hematopoietic stem cell population that contribute to emergent megakaryopoiesis.International journal of hematology · 2022Article
- Platelets in the neonate: Not just a small adult.Research and practice in thrombosis and haemostasis · 2022Article
- Podoplanin: Its roles and functions in neurological diseases and brain cancers.Frontiers in pharmacology · 2022Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
During early embryonic development in mammals, including humans and mice, megakaryocytes (Mks) first originate from primitive hematopoiesis in the yolk sac. These embryonic Mks (eMks) circulate in the vasculature with unclear function. Herein, we report that podoplanin (PDPN), the ligand of C-type lectin-like receptor (CLEC-2) on Mks/platelets, is temporarily expressed in neural tissue during midgestation in mice. Loss of PDPN or CLEC-2 resulted in aneurysms and spontaneous hemorrhage, specifically in the lower diencephalon during midgestation. Surprisingly, more eMks/platelets had enhanced granule release and localized to the lower diencephalon in mutant mouse embryos than in wild-type littermates before hemorrhage. We found that PDPN counteracted the collagen-1-induced secretion of angiopoietin-1 from fetal Mks, which coincided with enhanced TIE-2 activation in aneurysm-like sprouts of PDPN-deficient embryos. Blocking platelet activation prevented the PDPN-deficient embryo from developing vascular defects. Our data reveal a new role for PDPN in regulating eMk function during midgestation.
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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.