© 1997 American Heart Association, Inc.
Articles |
Pulsatile Stretch Stimulates Superoxide Production and Activates Nuclear Factor-
B in Human Coronary Smooth Muscle
From Cardiology, Cardiovascular Research, University Hospitals, Bern and Zürich, Switzerland, and the Institute of Physiology, University Zürich.
Correspondence to Thomas F. Lüscher, MD, FACC, FESC, Professor and Head of Cardiology, University Hospital, CH-8091 Zürich, Switzerland.
Abstract There is increasing evidence that oxidative
stress is of pathophysiological importance in
cardiovascular disease. Mechanical forces such as
pulsatility may also contribute. Using human coronary artery
smooth muscle cells (HCAS), we tested the hypothesis that
stretch-induced cell proliferation is associated with oxidative stress.
Stretch induced DNA synthesis in HCAS, and this was prevented by the
antioxidants N-acetylcysteine and pyrrolidinedithiocarbamate
(PDTC). Pulsatile stretch also increased superoxide production
from HCAS in a time- and stretch-dependent manner. Stretch-induced
superoxide production was inhibited by
diphenyleneiodoniumchloride, an NADPH oxidase inhibitor,
and p-chloromercuriphenylsulfonic acid, an NADH oxidase
inhibitor, but not by the xanthine oxidase
inhibitor oxypurinol or the
cyclooxygenase inhibitor
indomethacin. In electrophoretic mobility shift assays,
tumor necrosis factor-
activated nuclear factor-B
(NF-B) with a peak at 
3 hours, whereas pulsatile stretch showed
sustained activation during stimulation for up to 24 hours. The
sustained activation of NF-B was abolished by cotreatment with
N-acetylcysteine or PDTC. Furthermore, treatment of HCAS
with antisense p65 and p50 oligodeoxynucleotides of NF-B
inhibited stretch-induced DNA synthesis. We propose that pulsatile
stretch increases oxidative stress and, in turn, promotes DNA synthesis
via NF-B in cultured human coronary artery smooth muscle
cells.
Key Words: superoxide • stretch • nuclear factor-B • antisense • NADPH oxidase
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