Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:3570-3577
© 1997 American Heart Association, Inc.
Articles |
Reactive Oxygen Species Are Involved in Shear Stress-Induced Intercellular Adhesion Molecule-1 Expression in Endothelial Cells
From the Institute of Biomedical Sciences–Academia Sinica, and Graduate Institute for Life Sciences (B.S.W.), National Defense Medical Center, and Department of Chemical Engineering, National Taiwan University (H.J.H.), Taipei, Taiwan, ROC.
Correspondence to Dr Jeng-Jiann Chiu, Cardiovascular Division, Institute of Biomedical Sciences, Academia Sinica, Taipei, 11529, Taiwan, ROC.
Abstract Vascular endothelial cells (ECs) are
constantly subjected to flow-induced shear stress. Although the effects
of shear stress on ECs are well known, the intracellular signal
mechanisms remain largely unclear. Reactive oxygen species (ROS) have
recently been suggested to act as intracellular second messengers. The
potential role of ROS in shear-induced gene expression was examined in
the present study by subjecting ECs to a shear force using a
parallel-plate flow chamber system. ECs under shear flow increased
their intracellular ROS as indicated by superoxide production.
This superoxide production was maintained at an elevated
level as shear flow remained. Sheared ECs, similar to
TNF
-, PMA-, or H2O2-treated
cells, increased their intercellular adhesion molecule-1 (ICAM-1) mRNA
levels in a time-dependent manner. Pretreatment of ECs with an
antioxidant, N-acetyl-cysteine (NAC) or catalase, inhibited
this shear-induced or oxidant-induced ICAM-1 expression. ROS that were
involved in the shear-induced ICAM-1 gene expression were further
substantiated by functional analysis using a chimera containing
the ICAM-1 promoter region (-850 bp) and the reporter gene luciferase.
Shear-induced promoter activities were attenuated by pretreating
sheared ECs with NAC and catalase. Flow cytometric analysis and
monocytic adhesion assay confirmed the inhibitory effect of
NAC and catalase on the shear-induced ICAM-1 expression on ECs. These
results clearly demonstrate that shear flow to ECs can induce
intracellular ROS generation that may result in an increase of ICAM-1
mRNA levels via transcriptional events. Our findings thus support the
importance of intracellular ROS in modulating
hemodynamically induced endothelial
responses.
Key Words: endothelial cells • ICAM-1 • reactive oxygen species • shear stress
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