Genetic Reduction of Vascular Endothelial Growth Factor Receptor 2 Rescues Aberrant Angiogenesis Caused by Epsin Deficiency
Author(s) -
Kandice L. Tessneer,
Satish Pasula,
Xiaofeng Cai,
Yunzhou Dong,
John McManus,
Xiaolei Liu,
Lili Yu,
Scott Hahn,
Baojun Chang,
Yiyuan Chen,
Courtney T. Griffin,
Lijun Xia,
Ralf H. Adams,
Hong Chen
Publication year - 2013
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.113.302586
Subject(s) - angiogenesis , biology , kinase insert domain receptor , downregulation and upregulation , vascular endothelial growth factor , microbiology and biotechnology , angiogenesis inhibitor , endothelial stem cell , embryonic stem cell , cancer research , vascular endothelial growth factor a , vegf receptors , in vitro , genetics , gene
We previously showed that endothelial epsin deficiency caused elevated vascular endothelial growth factor receptor 2 (VEGFR2) and enhanced VEGF signaling, resulting in aberrant tumor angiogenesis and reduced tumor growth in adult mice. However, direct evidence demonstrating that endothelial epsins regulate angiogenesis specifically through VEGFR2 downregulation is still lacking. In addition, whether the lack of epsins causes abnormal angiogenesis during embryonic development remains unclear.
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