CCBE1 Enhances Lymphangiogenesis via A Disintegrin and Metalloprotease With Thrombospondin Motifs-3–Mediated Vascular Endothelial Growth Factor-C Activation
Author(s) -
Michael Jeltsch,
Sawan Kumar Jha,
Denis Tvorogov,
Andrey Anisimov,
VeliMatti Leppänen,
Tanja Holopainen,
Riikka Kivelä,
Sagrario Ortega,
Terhi Kärpänen,
Kari Alitalo
Publication year - 2014
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/circulationaha.113.002779
Subject(s) - lymphangiogenesis , vascular endothelial growth factor c , angiogenesis , biology , vascular endothelial growth factor , disintegrin , vascular endothelial growth factor b , microbiology and biotechnology , neuropilin 1 , cancer research , vascular endothelial growth factor a , growth factor , metalloproteinase , receptor , matrix metalloproteinase , genetics , metastasis , cancer , vegf receptors
Hennekam lymphangiectasia-lymphedema syndrome (Online Mendelian Inheritance in Man 235510) is a rare autosomal recessive disease, which is associated with mutations in the CCBE1 gene. Because of the striking phenotypic similarity of embryos lacking either the Ccbe1 gene or the lymphangiogenic growth factor Vegfc gene, we searched for collagen- and calcium-binding epidermal growth factor domains 1 (CCBE1) interactions with the vascular endothelial growth factor-C (VEGF-C) growth factor signaling pathway, which is critical in embryonic and adult lymphangiogenesis.
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