Relationship between epidermal growth factor-like domain 7 and angiogenesis in atherosclerotic plaques
10.3760/cma.j.issn.0254-9026.2012.01.014
- VernacularTitle:类表皮生长因子域7与动脉粥样硬化斑块内血管生成关系
- Author:
Weidong JIANG
;
Jiping ZENG
;
Yusheng LIU
;
Xin WANG
;
Aiqiong QIN
;
Qinghua LU
;
Zhiming GE
- Publication Type:Journal Article
- Keywords:
RNA,small interfering;
Atherosclerosis;
Angiogenesis inducing
- From:
Chinese Journal of Geriatrics
2012;31(1):39-43
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the expression of epidermal growth factor-like domain 7 (Egfl7) in atherosclerotic plaques and effects of its small interference RNA (siRNA) on angiogenesis gene expression in human endothelial cell line (HUVEC). MethodsEgfl7 expression in atheroscleroticplaquesweredetectedinhumaniliacarteryandmousearteriaeusing immunohistochemistry and immunofluorescence stainings.The siRNA targeting Egfl7 was transfected into HUVEC by lipofectamine with non-transfected cells and unconcerned siRNA as controls.At 0 h,12 h,24 h and 48 h after intervention,the levels of mRNA and protein of Egf17,vascular endothelial growth factor(VEGF),platelet derived growth factor-A (PDGF-A),platelet derived growth factor-B (PDGF-B),vascular cell adhesion molecule(VCAM) and intercellular adhesion molecule (ICAM)were measured by RT-PCR and Western blotting,respectively. ResultsThe expressions of Egfl7 in human iliac artery and mouse arteriae were increased.The expressions of Egfl7 in HUVEC at the levels of mRNA were[(0.14±0.02),(0.09±0.01),(0.02±0.01)]and the levels of protein[(0.71±0.11),(0.39±0.09),(0.07±0.01)]at 12 h,24 h and 48 h after siRNA intervention,respectively,which were decreased as compared with 0 h intervention [(0.31 ±0.05) and (0.93±0.08) ].Other genes such as VEGF,PDGF-A and PDGF-B were reduced or silenced at the levels of protein and mRNA in HUVEC with siRNA longer interventions(all P＜0.05).ConclusionsThe expression of Egfl7 in atherosclerotic plaques is increased.The siRNA inhibiting Egfl7 gene expression results in silence of other factors involved in angiogenesis.
