ArticleThe Journal of clinical investigation2008
Endothelial cell O-glycan deficiency causes blood/lymphatic misconnections and consequent fatty liver disease in mice.
Article in The Journal of clinical investigation, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 136 papers.
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Who cites it
136 citing papers in PubMed, 240 citations in OpenAlex.
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- O-GalNAc glycans are enriched in neuronal tracts and regulate nodes of Ranvier.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
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- Endothelial Slc35a1 Deficiency Causes Loss of LSEC Identity and Exacerbates Neonatal Lipid Deposition in the Liver in Mice.Cellular and molecular gastroenterology and hepatology · 2024Article
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- Reduction in disialyl-T antigen levels in mice deficient for both St6galnac3 and St6galnac4 results in blood filling of lymph nodes.Scientific reports · 2023Article
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- GATA2 regulates blood/lymph separation in a platelet-dependent and lymphovenous valve-independent manner.Microcirculation (New York, N.Y. : 1994) · 2023Article
- Lymphatic/blood vessel plasticity: motivation for a future research area based on present and past observations.American journal of physiology. Heart and circulatory physiology · 2023Review
- Human Dectin-1 iseLife · 2022Article
- Podoplanin is Responsible for the Distinct Blood and Lymphatic Capillaries.Cellular and molecular bioengineering · 2022Article
- Translational Value of Tumor-Associated Lymphangiogenesis in Cholangiocarcinoma.Journal of personalized medicine · 2022Review
- In vivo models of mucin biosynthesis and function.Advanced drug delivery reviews · 2022Review
76 more citing papers are in PubMed but not listed here.
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
Abstract
Mucin-type O-glycans (O-glycans) are highly expressed in vascular ECs. However, it is not known whether they are important for vascular development. To investigate the roles of EC O-glycans, we generated mice lacking T-synthase, a glycosyltransferase encoded by the gene C1galt1 that is critical for the biosynthesis of core 1-derived O-glycans, in ECs and hematopoietic cells (termed here EHC T-syn(-/-) mice). EHC T-syn(-/-) mice exhibited embryonic and neonatal lethality associated with disorganized and blood-filled lymphatic vessels. Bone marrow transplantation and EC C1galt1 transgene rescue demonstrated that lymphangiogenesis specifically requires EC O-glycans, and intestinal lymphatic microvessels in EHC T-syn(-/-) mice expressed a mosaic of blood and lymphatic EC markers. The level of O-glycoprotein podoplanin was significantly reduced in EHC T-syn(-/-) lymphatics, and podoplanin-deficient mice developed blood-filled lymphatics resembling EHC T-syn(-/-) defects. In addition, postnatal inactivation of C1galt1 caused blood/lymphatic vessel misconnections that were similar to the vascular defects in the EHC T-syn(-/-) mice. One consequence of eliminating T-synthase in ECs and hematopoietic cells was that the EHC T-syn(-/-) pups developed fatty liver disease, because of direct chylomicron deposition via misconnected portal vein and intestinal lymphatic systems. Our studies therefore demonstrate that EC O-glycans control the separation of blood and lymphatic vessels during embryonic and postnatal development, in part by regulating podoplanin expression.
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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.