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COUP‐TFII switches responses of venous endothelium to atherosclerotic factors through controlling the profile of various inherent genes expression
Author(s) -
Wu Xiaojing,
Zou Yunzeng,
Liang Yanyan,
Zhou Qi,
Gong Hui,
Sun Aijun,
Yuan Lingyan,
Wang Keqiang,
Ge Junbo
Publication year - 2011
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.22923
Subject(s) - gene knockdown , transfection , biology , downregulation and upregulation , angiotensin ii , endothelial stem cell , transcription factor , microbiology and biotechnology , gene , medicine , endocrinology , in vitro , genetics , blood pressure
Endothelial cells of arteries (AEC) have a strikingly greater responsiveness to atherosclerosis factors than venous endothelial cells (VEC). However, the reasons for this phenomenon remain unclear. Chicken ovalbumin upstream promoter‐transcription factor II (COUP‐TFII) plays an important role in regulating embryonic arterial‐venous differentiation. We therefore investigate whether COUP‐TFII is related to this different susceptibility between AEC and VEC. It is first confirmed that COUP‐TFII is expressed in VEC but not in AEC in the adult. Using a siRNA strategy, we identified the expression of Jagged1 and Notch1 in cultured human VEC, which usually exist only in AEC, after knocking down of COUP‐TFII. To further elucidate the role of COUP‐TFII, we performed DNA microarrays in VEC transfected with the siRNA of COUP‐TFII and subsequently stimulated with angiotensin II (AngII) and compared the expression profiles of 112 genes involved in various atherosclerosis‐related pathways. The results indicated that expression of atherogenic genes was significantly upregulated after AngII stimulation in VEC transfected with COUP‐TFII siRNA. Moreover, in vitro cell functional assay showed that knockdown of COUP‐TFII in VEC increased not only basal but also AngII‐induced cell adhesions. These results demonstrate that COUP‐TFII suppresses the susceptibility of VEC to atherosclerosis through controlling the expression of various atherosclerosis‐related molecules. J. Cell. Biochem. 112: 256–264, 2011. © 2010 Wiley‐Liss, Inc.