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Loss of osteoglycin promotes angiogenesis in limb ischaemia mouse models via modulation of vascular endothelial growth factor and vascular endothelial growth factor receptor 2 signalling pathway

文献类型：期刊论文

作者Wu, Qi-Hong1; Ma, Yu1; Ruan, Cheng-Chao1; Yang, Yan1,4; Liu, Xin-He1; Ge, Qian1,4; Kong, Ling-Ran1,4; Yan, Chen1,4; Gao, Ping-Jin1,2,3,4; Ruan, Cheng-Chao2,3,4
刊名CARDIOVASCULAR RESEARCH
出版日期2017
卷号113期号:1页码:70-80
关键词Osteoglycin Angiogenesis Extracellular matrix VEGF VEGFR2
ISSN号0008-6363
DOI10.1093/cvr/cvw220
文献子类Article
英文摘要Objective Osteoglycin (OGN) has been noted for its implication in cardiovascular disease in recent studies. However, the relationship between OGN and angiogenesis remains unknown. Therefore, we aimed to investigate the effect of OGN on ischaemia-induced angiogenesis and to address the underlying mechanisms. Methods and results The expression of OGN was decreased in a limb ischaemia mouse model. OGN knockout (KO) mice were used to further understand the role of OGN after ischaemia. The perfusion recovery rate after femoral artery ligation was higher in OGN KO mice than in wild-type (WT) mice. The capillary density in the gastrocnemius muscle of the ischaemic limb was also higher in OGN KO mice. Moreover, ex vivo aortic ring explants from OGN KO mice exhibited stronger angiogenic sprouting than those from WT mice. In human umbilical vein endothelial cells (HUVECs), OGN knockdown enhanced endothelial cell (EC) activation, including tube formation, proliferation, and migration. In contrast, OGN overexpression inhibited HUVEC activation. Mechanistic studies revealed that OGN associates with vascular endothelial growth factor receptor 2 (VEGFR2) and negatively regulates the interaction of vascular endothelial growth factor (VEGF) and VEGFR2, thereby negatively modulating the activation of VEGFR2 and its downstream signalling pathways. Consistently, the pro-angiogenic effect of OGN KO was abrogated by VEGFR2 inhibition, supporting the critical role of VEGFR2 signalling in OGN-mediated regulation of angiogenic function. Conclusions OGN plays a critical role in negatively regulating ischaemia-induced angiogenesis by inhibiting VEGF-VEGFR2 signalling and thereby attenuating EC tube formation, proliferation, and migration. Thus, OGN may be a novel therapeutic target for ischaemic vascular diseases.
学科主题Cardiovascular System & Cardiology
WOS关键词THERAPEUTIC ANGIOGENESIS ; ATHEROSCLEROTIC PLAQUES ; EXTRACELLULAR-MATRIX ; CLINICAL-TRIALS ; DISEASE ; EXPRESSION ; AUTOPHAGY ; DECORIN ; MUSCLE ; CELLS
语种英语
WOS记录号WOS:000397023400012
出版者OXFORD UNIV PRESS
版本出版稿
源URL[http://202.127.25.144/handle/331004/1314]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Shanghai Jiao Tong Univ, Ruijin Hosp, Sch Med, Dept Hypertens,State Key Lab Med Gen, Shanghai 200025, Peoples R China;
2.Chinese Acad Sci, Inst Hlth Sci, Shanghai Inst Biol Sci, Lab Vasc Biol & Key Lab Stem Cell Biol, Shanghai, Peoples R China;
3.Shanghai Jiao Tong Univ, Sch Med, Shanghai, Peoples R China;
4.Shanghai Res Inst Hypertens, Shanghai 200025, Peoples R China;
5.Shanghai Jiao Tong Univ, Renji Hosp, Sch Med, Shanghai 200127, Peoples R China,
推荐引用方式
GB/T 7714		 Wu, Qi-Hong,Ma, Yu,Ruan, Cheng-Chao,et al. Loss of osteoglycin promotes angiogenesis in limb ischaemia mouse models via modulation of vascular endothelial growth factor and vascular endothelial growth factor receptor 2 signalling pathway[J]. CARDIOVASCULAR RESEARCH,2017,113(1):70-80.
APA Wu, Qi-Hong.,Ma, Yu.,Ruan, Cheng-Chao.,Yang, Yan.,Liu, Xin-He.,...&,.(2017).Loss of osteoglycin promotes angiogenesis in limb ischaemia mouse models via modulation of vascular endothelial growth factor and vascular endothelial growth factor receptor 2 signalling pathway.CARDIOVASCULAR RESEARCH,113(1),70-80.
MLA Wu, Qi-Hong,et al."Loss of osteoglycin promotes angiogenesis in limb ischaemia mouse models via modulation of vascular endothelial growth factor and vascular endothelial growth factor receptor 2 signalling pathway".CARDIOVASCULAR RESEARCH 113.1(2017):70-80.

入库方式： OAI收割

来源：上海营养与健康研究所

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