ArticleCardiovascular research2016
Endothelial lipid phosphate phosphatase-3 deficiency that disrupts the endothelial barrier function is a modifier of cardiovascular development.
Article in Cardiovascular research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Ox-LDL induces a non-inflammatory response enriched for coronary artery disease risk in human endothelial cells.Scientific reports · 2025Article
- LncRNA SNHG15 promotes angiogenesis and improves cardiac repair after myocardial infarction through MiR-665-mediated KDR expression.Cellular and molecular life sciences : CMLS · 2025Article
- Kindlin-3 Promotes Angiogenesis via Notch Signalling and Is Crucial for Functional Recovery Postmyocardial Infarction.Journal of cellular and molecular medicine · 2025Article
- From Classical to Alternative Pathways of 2-Arachidonoylglycerol Synthesis: AlterAGs at the Crossroad of Endocannabinoid and Lysophospholipid Signaling.Molecules (Basel, Switzerland) · 2024Review
- Lipid phosphate phosphatase 3 maintains NO-mediated flow-mediated dilatation in human adipose resistance arterioles.The Journal of physiology · 2023Article
- Plpp3, a novel regulator of pluripotency exit and endodermal differentiation of mouse embryonic stem cells.Biology open · 2023Article
- Sphingosine 1-phosphate receptor-targeted therapeutics in rheumatic diseases.Nature reviews. Rheumatology · 2022Review
- Nogo-B promotes angiogenesis and improves cardiac repair after myocardial infarction via activating Notch1 signaling.Cell death & disease · 2022Article
- A requirement for Krüppel Like Factor-4 in the maintenance of endothelial cell quiescence.Frontiers in cell and developmental biology · 2022Article
- Lysolipids in Vascular Development, Biology, and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Low-Level Nanog Expression in the Regulation of Quiescent Endothelium.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Coronary Artery Disease Risk-AssociatedArteriosclerosis, thrombosis, and vascular biology · 2019Article
- Bioactive lysolipids in cancer and angiogenesis.Pharmacology & therapeutics · 2019Review
- Cardiac-specific inactivation of LPP3 in mice leads to myocardial dysfunction and heart failure.Redox biology · 2018Article
- Review
- Chromatin-modifying agents convert fibroblasts to OCT4+ and VEGFR-2+ capillary tube-forming cells.PloS one · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
aimsLipid phosphate phosphatase-3 (LPP3) is expressed at high levels in endothelial cells (ECs). Although LPP3 is known to hydrolyse the phosphate group from lysolipids such as spingosine-1-phosphate and its structural homologues, the function of Lpp3 in ECs is not completely understood. In this study, we investigated how tyrosine-protein kinase receptor (TEK or Tie2) promoter-dependent deletion of Lpp3 alters EC activities. METHODS AND
resultsLpp3(fl/fl) mice were crossed with the tg.Tie2(Cre) transgenic line. Vasculogenesis occurred normally in embryos with Tie2(Cre)-mediated deletion of Lpp3 (called Lpp3(ECKO)), but embryonic lethality occurred in two waves, the first wave between E8.5 and E10.5, while the second between E11.5 and E13.5. Lethality in Lpp3(ECKO) embryos after E11.5 was accompanied by vascular leakage and haemorrhage, which likely resulted in insufficient cardiovascular development. Analyses of haematoxylin- and eosin-stained heart sections from E11.5 Lpp3(ECKO) embryos showed insufficient heart growth associated with decreased trabeculation, reduced growth of the compact wall, and absence of cardiac cushions. Staining followed by microscopic analyses of Lpp3(ECKO) embryos revealed the presence of apoptotic ECs. Furthermore, Lpp3-deficient ECs showed decreased gene expression and protein levels of Cyclin-D1, VE-cadherin, Fibronectin, Klf2, and Klf4. To determine the underlying mechanisms of vascular leakage and barrier disruption, we performed knockdown and rescue experiments in cultured ECs. LPP3 knockdown decreased transendothelial electrical resistance and increased permeability. Re-expression of β-catenin cDNA in LPP3-knockdown ECs partially restored the effect of the LPP3 loss, whereas re-expression of p120ctn cDNA did not.
conclusionThese findings demonstrate the essential roles of LPP3 in the maturation of EC barrier integrity and normal cardiovascular development.
Indexed as
Identifiers
What OpenQuestion holds
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.