@Article{mcb.2017.014.197, AUTHOR = {Bo Ling, Daoxi Lei, Juhui Qiu, Kang Zhang, Hao Chen, Yeqi Wang, Zhiyi Ye, Guixue Wang}, TITLE = {Shear Stress and Oxidized LDL Regulates Endothelial Cell Tube Formation through VEGF Signaling}, JOURNAL = {Molecular \& Cellular Biomechanics}, VOLUME = {14}, YEAR = {2017}, NUMBER = {4}, PAGES = {197--211}, URL = {http://www.techscience.com/mcb/v14n4/28607}, ISSN = {1556-5300}, 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.}, DOI = {10.3970/mcb.2017.014.197} }