Protective role of shear flow in inflammatory agent-stimulated vascular endothelial cells: Regulation of interferon-induced Stat1 signaling and related gene expression by shear flow(1/3)
Date Issued
2005
Date
2005
Author(s)
DOI
932321B002034
Abstract
Endothelial cells (ECs) are constantly exposed
to blood flow-induced shear stress. Laminar shear
stress protects ECs from endothelial dysfunction.
In the present study, the effect of shear stress (SS)
on IFN摯瑬敳獩 -induced responses including STAT1 and
JAK1/2 phosphorylation in ECs was examined.
SS had no effect on Tyr701 and Ser727
phosphorylation of STAT1 in ECs under basal
condition. Further, IFN摯瑬敳獩 triggered the activation
of JAK/STAT1 signaling pathway with the
phosphorylation of JAK1/2 and phosphorylation
of Tyr701 and Ser727 in STAT1. Under
IFN摯瑬敳獩 treatment, Tyr-701 phosphorylation
approached the highest level at 30 minutes and
Ser-727 phosphorylation obviously rised after 30
minutes. IFN摯瑬敳獩 induced Tyr-701 and Ser-727
phosphorylation in a dose-dependent manner,
which Tyr-701 and Ser-727 phosphorylation
approached their highest levels with IFN摯瑬敳獩
concentration of 2.5 ng/ml. When SS was applied
to IFN摯瑬敳獩 -treated ECs, it significantly inhibited the
IFN摯瑬敳獩 -induced Tyr701 phosphorylation of STAT1
in a shear force- and time course-dependent
manner whiles Ser727 phosphorylation was unaffected. IFN摯瑬敳獩 , through STAT1 signaling
pathway, induced downstream chemokine IP-10
expression. Whether SS affects IFN摯瑬敳獩 -induced
downstream target gene expressions will be
examined in the future study. To sum up, our
results demonstrated that SS attenuates
IFN摯瑬敳獩 -induced JAK1/2 and STAT1 activation that
will provide a protective effect on ECs during
inflammatory response.
Subjects
shear stress
endothelial cells
cytokine
chemokine
Publisher
臺北市：國立臺灣大學化學工程學系暨研究所
Type
report
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