ArticleArteriosclerosis, thrombosis, and vascular biology2013
Lipid phosphate phosphatase 3 negatively regulates smooth muscle cell phenotypic modulation to limit intimal hyperplasia.
Article in Arteriosclerosis, thrombosis, and vascular biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 50 citations in OpenAlex.
- Molecular subtypes of vascular endothelial cell differentiation in keloid by single-cell sequencing.Chinese medical journal · 2026Article
- Decoding lysophosphatidic acid signaling in physiology and disease: mapping the multimodal and multinodal signaling networks.Signal transduction and targeted therapy · 2025Review
- Early reduction of skin potassium without sodium accumulation in the pathogenesis of salt sensitivity in primary aldosteronism.Frontiers in pharmacology · 2025Article
- Protein interaction networks in the vasculature prioritize genes and pathways underlying coronary artery disease.Communications biology · 2024Article
- The Autotaxin-LPA Axis Emerges as a Novel Regulator of Smooth Muscle Cell Phenotypic Modulation during Intimal Hyperplasia.International journal of molecular sciences · 2023Article
- Lipid phosphate phosphatase 3 maintains NO-mediated flow-mediated dilatation in human adipose resistance arterioles.The Journal of physiology · 2023Article
- Alteration of Cellular Energy Metabolism through LPAR2-Axin2 Axis in Gastric Cancer.Biomolecules · 2022Article
- Bioactive lipids and metabolic syndrome-a symposium report.Annals of the New York Academy of Sciences · 2022Article
- Lipid phosphate phosphatase 3 in smooth muscle cells regulates angiotensin II-induced abdominal aortic aneurysm formation.Scientific reports · 2022Article
- Uncovering the 'sphinx' of sphingosine 1-phosphate signalling: from cellular events to organ morphogenesis.Biological reviews of the Cambridge Philosophical Society · 2022Review
- Loss of FoxO3a prevents aortic aneurysm formation through maintenance of VSMC homeostasis.Cell death & disease · 2021Article
- Coronary Artery Disease Risk-AssociatedArteriosclerosis, thrombosis, and vascular biology · 2019Article
- Regulation of PLPP3 gene expression by NF-κB family transcription factors.The Journal of biological chemistry · 2019Article
- Integrated Human Evaluation of the Lysophosphatidic Acid Pathway as a Novel Therapeutic Target in Atherosclerosis.Molecular therapy. Methods & clinical development · 2018Article
- Study of the association of 17 lipid-related gene polymorphisms with coronary heart disease.Anatolian journal of cardiology · 2018Article
- Article
- Liver-specific deletion of the Plpp3 gene alters plasma lipid composition and worsens atherosclerosis in apoEScientific reports · 2017Article
- Different origins of lysophospholipid mediators between coronary and peripheral arteries in acute coronary syndrome.Journal of lipid research · 2017Article
- Role of lipid phosphate phosphatase 3 in human aortic endothelial cell function.Cardiovascular research · 2016Article
- Endothelial lipid phosphate phosphatase-3 deficiency that disrupts the endothelial barrier function is a modifier of cardiovascular development.Cardiovascular research · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
objectiveThe lipid phosphate phosphatase 3 (LPP3) degrades bioactive lysophospholipids, including lysophosphatidic acid and sphingosine-1-phosphate, and thereby terminates their signaling effects. Although emerging evidence links lysophosphatidic acid to atherosclerosis and vascular injury responses, little is known about the role of vascular LPP3. The goal of this study was to determine the role of LPP3 in the development of vascular neointima formation and smooth muscle cells (SMC) responses. METHODS AND
resultsWe report that LPP3 is expressed in vascular SMC after experimental arterial injury. Using gain- and loss-of-function approaches, we establish that a major function of LPP3 in isolated SMC cells is to attenuate proliferation (extracellular signal-regulated kinases) activity, Rho activation, and migration in response to serum and lysophosphatidic acid. These effects are at least partially a consequence of LPP3-catalyzed lysophosphatidic acid hydrolysis. Mice with selective inactivation of LPP3 in SMC display an exaggerated neointimal response to injury.
conclusionsOur observations suggest that LPP3 serves as an intrinsic negative regulator of SMC phenotypic modulation and inflammation after vascular injury, in part, by regulating lysophospholipid signaling. These findings may provide a mechanistic link to explain the association between a PPAP2B polymorphism and coronary artery disease risk.
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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.