Premium
Oscillatory shear stress promotes endothelial cell migration and angiogenesis
Author(s) -
Tressel Sarah L,
Huang RuoPan,
Jo Hanjoong
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.4.a289
Subject(s) - angiogenesis , umbilical vein , matrigel , cell migration , endothelial stem cell , downregulation and upregulation , neovascularization , arteriogenesis , microbiology and biotechnology , chemistry , cancer research , biology , gene , cell , biochemistry , in vitro
Increased angiogenesis has been found in atherosclerotic plaques suggesting a role for angiogenesis in atherosclerosis development. Atherosclerosis occurs in arterial regions exposed to oscillatory shear stress (OS) such as at branches whereas arterial regions exposed to laminar shear stress (LS) are protected from atherosclerosis. Here, we investigated the effects of shear stress on endothelial cell (EC) migration and angiogenesis. We hypothesize that OS promotes EC dysfunction leading to EC destabilization and activation to migrate and increase production of angiogenic mediators, thus leading to plaque angiogenesis. To test this hypothesis, human umbilical vein ECs (HUVECs) subjected to either LS (15 dynes/cm 2 ) or OS (± 5 dynes/cm 2 ) for 24 hours were used in Matrigel tube formation, scratch and Transwell filter migration assays. HUVECs exposed to OS were found to have increased migration and tube formation as compared to LS. To identify a mechanism, we performed a gene array of 128 human angiogenic genes and a protein array of 60 human cytokines. We found 3 genes and 8 proteins upregulated by OS compared to LS, and 16 genes and 2 proteins downregulated by OS compared to LS (P<0.05). Of interest, angiopoietin 2, a known angiogenic gene, was upregulated by OS both at the RNA and protein level. Our data suggests that OS promotes EC migration and angiogenesis, which may play a role in plaque angiogenesis. Supported by NIH.