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Mice With Targeted Inactivation of Ppap2b in Endothelial and Hematopoietic Cells Display Enhanced Vascular Inflammation and Permeability
Author(s) -
Manikandan Panchatcharam,
Abdel Salous,
J. Anthony Brandon,
Sumitra Miriyala,
Jessica Wheeler,
Pooja Patil,
Manjula Sunkara,
Andrew J. Morris,
Diana EscalanteAlcalde,
Susan S. Smyth
Publication year - 2014
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.113.302335
Subject(s) - lysophosphatidic acid , autotaxin , inflammation , vascular permeability , biology , microbiology and biotechnology , cancer research , immunology , receptor , endocrinology , biochemistry
Lipid phosphate phosphatase 3 (LPP3), encoded by the PPAP2B gene, is an integral membrane enzyme that dephosphorylates, and thereby terminates, the G-protein-coupled receptor-mediated signaling actions of lysophosphatidic acid (LPA) and sphingosine-1-phosphate. LPP3 is essential for normal vascular development in mice, and a common PPAP2B polymorphism is associated with increased risk of coronary artery disease in humans. Herein, we investigate the function of endothelial LPP3 to understand its role in the development and human disease.

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