Inhibition of vascular permeability factor/vascular endothelial growth factor-mediated angiogenesis by the Kruppel-like factor KLF2

被引：148

作者：

Bhattacharya, R

SenBanerjee, S

Lin, ZY

Mir, S

Hamik, A

Wang, P

Mukherjee, P

Mukhopadhyay, D

Jain, MK ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Brigham & Womens Hosp, Program Cardiovasc Transcriptional Biol, Boston, MA 02115 USA

[2] Mayo Clin & Mayo Fdn, Mayo Clin Canc Ctr, Rochester, MN 55905 USA

来源：

JOURNAL OF BIOLOGICAL CHEMISTRY | 2005年 / 280卷 / 32期

关键词：

D O I：

10.1074/jbc.C500200200

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

The Kruppel-like factor KLF2 was recently identified as a novel regulator of endothelial pro-inflammatory and pro-thrombotic function. Here it is shown that overexpression of KLF2 potently inhibits vascular permeability factor/vascular endothelial growth factor (VEGFA)mediated angiogenesis and tissue edema in the nude ear mouse model of angiogenesis. In vitro, KLF2 expression retards VEGF-mediated calcium flux, proliferation and induction of pro-inflammatory factors in endothelial cells. This effect is due to a potent inhibition of VEGFR2/KDR expression and promoter activity. These observations identify KLF2 as a regulator of VEGFR2/KDR and provide a foundation for novel approaches to regulate angiogenesis.

引用

页码：28848 / 28851

页数：4

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