ArticleBlood2014
Endothelial Smad4 restrains the transition to hematopoietic progenitors via suppression of ERK activation.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 26 citations in OpenAlex.
- Serine Hydroxymethyltransferase 2 Deficiency in the Hematopoietic System Disrupts Erythropoiesis and Induces Anemia in Murine Models.International journal of molecular sciences · 2024Article
- Autophagy regulates the maturation of hematopoietic precursors in the embryo.Nature communications · 2024Article
- Network pharmacology and experimental verification of the potential mechanism of Er-Xian decoction in aplastic anemia.Scientific reports · 2023Article
- Article
- Nupr1 Negatively Regulates Endothelial to Hematopoietic Transition in the Aorta-Gonad-Mesonephros Region.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- A positive feedback loop of ARF6 activates ERK1/2 signaling pathway viaActa biochimica et biophysica Sinica · 2022Article
- Regulation of Hemogenic Endothelial Cell Development and Function.Annual review of physiology · 2021Review
- Embryonic endothelial evolution towards first hematopoietic stem cells revealed by single-cell transcriptomic and functional analyses.Cell research · 2020Article
- The chromatin remodeling subunit Baf200 promotes normal hematopoiesis and inhibits leukemogenesis.Journal of hematology & oncology · 2018Article
- Let-7 microRNA-dependent control of leukotriene signaling regulates the transition of hematopoietic niche in mice.Nature communications · 2017Article
- Inductive interactions mediated by interplay of asymmetric signalling underlie development of adult haematopoietic stem cells.Nature communications · 2016Article
- SMAD1 and SMAD5 Expression Is Coordinately Regulated by FLI1 and GATA2 during Endothelial Development.Molecular and cellular biology · 2015Article
- Article
- Blood vascular abnormalities in Rasa1(R780Q) knockin mice: implications for the pathogenesis of capillary malformation-arteriovenous malformation.The American journal of pathology · 2014Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In mouse mid-gestational embryos, definitive hematopoietic stem progenitor cells are derived directly from a very small proportion of the arterial endothelium. However, the physiological mechanisms restraining excessive endothelial-hematopoietic transition remain elusive. We show here that genetic deletion of Smad4 from the endothelium stage (using Tie2-Cre), but not from embryonic hematopoietic cells (using Vav-Cre), leads to a strikingly augmented emergence of intra-arterial hematopoietic clusters and an enhanced in vitro generation of hematopoietic progenitors, with no increase in the proliferation and survival of hematopoietic cluster cells. This finding indicates a temporally restricted negative effect of Smad4 on the endothelial to hematopoietic progenitor transition. Furthermore, the absence of endothelial Smad4 causes an increased expression of subaortic bone morphogenetic protein 4 and an activation of aortic extracellular signal-regulated kinase, thereby resulting in the excessive generation of blood cells. Collectively, our data for the first time identify a physiological suppressor that functions specifically during the transition of endothelial cells to hematopoietic progenitors and further suggest that endothelial Smad4 is a crucial modulator of the subaortic microenvironment that controls the hematopoietic fate of the aortic endothelium.
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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.