ArticleMolecular and cellular biology2014
Fusing VE-cadherin to α-catenin impairs fetal liver hematopoiesis and lymph but not blood vessel formation.
Article in Molecular and cellular biology, 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, 22 citations in OpenAlex.
- VEGF-C and VE-cadherin: balancing sinusoidal and lymphatic angiogenesis.Nature cardiovascular research · 2022Article
- VEGF signaling and cell adhesion interplay controls sinusoidal and lymphatic growth.Nature cardiovascular research · 2022Article
- Sinusoidal and lymphatic vessel growth is controlled by reciprocal VEGF-C-CDH5 inhibition.Nature cardiovascular research · 2022Article
- Role of Transcriptional and Epigenetic Regulation in Lymphatic Endothelial Cell Development.Cells · 2022Review
- Force-induced changes of α-catenin conformation stabilize vascular junctions independently of vinculin.Journal of cell science · 2021Article
- Article
- Lymphatic Endothelial Cell Junctions: Molecular Regulation in Physiology and Diseases.Frontiers in physiology · 2020Review
- Distinct roles of VE-cadherin for development and maintenance of specific lymph vessel beds.The EMBO journal · 2018Article
- NBPF7 promotes the proliferation of α-catenin-knockdown HaCaT cells via functional interaction with the NF-κB pathway.Oncotarget · 2017Article
- GATA4-dependent organ-specific endothelial differentiation controls liver development and embryonic hematopoiesis.The Journal of clinical investigation · 2017Article
- Building discontinuous liver sinusoidal vessels.The Journal of clinical investigation · 2017Article
- DLL4 promotes continuous adult intestinal lacteal regeneration and dietary fat transport.The Journal of clinical investigation · 2015Article
- Reevaluating αE-catenin monomer and homodimer functions by characterizing E-cadherin/αE-catenin chimeras.The Journal of cell biology · 2015Article
- Nuclear signaling from cadherin adhesion complexes.Current topics in developmental biology · 2015Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have recently shown that genetic replacement of VE-cadherin by a VE-cadherin-α-catenin fusion construct strongly impairs opening of endothelial cell contacts during leukocyte extravasation and induction of vascular permeability in adult mice. Here we show that this mutation leads to lethality at midgestation on a clean C57BL/6 background. Investigating the reasons for embryonic lethality, we observed a lack of fetal liver hematopoiesis and severe lymphedema but no detectable defects in blood vessel formation and remodeling. As for the hematopoiesis defect, VE-cadherin-α-catenin affected neither the generation of hematopoietic stem and progenitor cells (HSPCs) from hemogenic endothelium nor their differentiation into multiple hematopoietic lineages. Instead, HSPCs accumulated in the fetal circulation, suggesting that their entry into the fetal liver was blocked. Edema formation was caused by disturbed lymphatic vessel development. Lymphatic progenitor cells of VE-cadherin-α-catenin-expressing embryos were able to leave the cardinal vein and migrate to the site of the first lymphatic vessel formation, yet subsequently, these cells failed to form large lumenized lymphatic vessels. Thus, stabilizing endothelial cell contacts by a covalent link between VE-cadherin and α-catenin affects recruitment of hematopoietic progenitors into the fetal liver and the development of lymph but not blood vessels.
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