ArticleArteriosclerosis, thrombosis, and vascular biology2023
eNOS Regulates Lymphatic Valve Specification by Controlling β-Catenin Signaling During Embryogenesis in Mice.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
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- A neuro-lymphatic communication guides lymphatic development by CXCL12 and CXCR4 signaling.Development (Cambridge, England) · 2024Article
- Zmiz1 is a novel regulator of lymphatic endothelial cell gene expression and function.PloS one · 2024Article
- Zmiz1 is a novel regulator of lymphatic endothelial cell gene expression and function.bioRxiv : the preprint server for biology · 2023Article
- Transplantation of engineered vascularized lymphatic tissue using LEC and in vivo AV loop model to enhance lymphangiogenesis and restore lymphatic drainage in a lymphadenectomy rat model.Journal of tissue engineeringArticle
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundLymphatic valves play a critical role in ensuring unidirectional lymph transport. Loss of lymphatic valves or dysfunctional valves are associated with several diseases including lymphedema, lymphatic malformations, obesity, and ileitis. Lymphatic valves first develop during embryogenesis in response to mechanotransduction signaling pathways triggered by oscillatory lymph flow. In blood vessels, eNOS (endothelial NO synthase; gene name:
methodsWe used global
resultsOur data reveal a 45% reduction in lymphatic valve specification cell clusters and that loss of eNOS protein inhibited activation of β-catenin and its nuclear translocation. Genetic knockout or knockdown of eNOS led to downregulation of β-catenin target proteins in vivo and in vitro. However, pharmacological inhibition of NO production did not reproduce these effects. Co-immunoprecipitation and proximity ligation assays reveal that eNOS directly binds to β-catenin and their binding is enhanced by oscillatory shear stress. Finally, genetic ablation of the
conclusionsIn conclusion, we demonstrate a novel, NO-independent role for eNOS in regulating lymphatic valve specification and propose a mechanism by which eNOS directly binds β-catenin to regulate its nuclear translocation and thereby transcriptional activity.
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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 Socratic graph.