Open Access

ARTICLE

Shear Stress and Oxidized LDL Regulates Endothelial Cell Tube Formation through VEGF Signaling

Bo Ling^1,#, Daoxi Lei^1,#, Juhui Qiu¹, Kang Zhang¹, Hao Chen^2,*, Yeqi Wang¹, Zhiyi Ye¹, Guixue Wang^*

1 Key Laboratory for Biorheological Science and Technology of Ministry of Education, State and Local Joint Engineering Laboratory for Vascular Implants, Bioengineering College of Chongqing University, Chongqing, 400044, China.
2 Cardiovascular Surgery Department of Chongqing General Hospital, Chongqing, 400013, China.
* Corresponding author: Guixue Wang. Email: wanggx@cqu.edu.cn;
Hao Chen. Email: cqchenhao@aliyun.com
# These two authors share the same contribution to this work.

Molecular & Cellular Biomechanics 2017, 14(4), 197-211. https://doi.org/10.3970/mcb.2017.014.197

Abstract

Shear stress and oxidized low-density lipoprotein (oxLDL) caused by abnormal blood is critical to angiogenesis for atherosclerosis. However, the mechanism in shear stress or ox-LDL regulated angiogenesis is still not well understood. There is the hypothesis that shear stress or oxLDL regulates angiogenesis through the vascular endothelial growth factor (VEGF) signaling pathway. It is discovered that both high shear stress and low concentration of oxLDL contribute to angiogenesis, which is inhibited once the VEGF or VEGFR expression is knocked down. The expression of p-FAK and p-paxillin is regulated by the VEGF/VEGFR signal axis. VEGFR2, p-FAK, p-paxillin and VEGFR1 are VEGF-responsive proteins, and they are also upregulated by high shear stress and low concentration of oxLDL. If the VEGF or VEGFR2 is knocked down, phosphorylation of FAK and paxillin induced by high shear stress and low concentration of oxLDL are also significantly inhibited. In summary, present studies have demonstrated that high shear stress and low concentration of oxLDL induces angiogenesis through the VEGFR2/FAK/paxillin signaling pathway.

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