© 2000 American Heart Association, Inc.
Cellular Biology |
Cyclooxygenase-2 Is Required for Tumor Necrosis Factor-
– and Angiotensin II–Mediated Proliferation of Vascular Smooth Muscle Cells
Presented in part at the 1998 Experimental Biology meeting in San Francisco, Calif, April 18–22, 1998, and published in abstract form (FASEB J. 1998;12:A403).
From the Department of Pharmacology, New York Medical College, Valhalla, NY.
Correspondence to Dr Nicholas R. Ferreri, Department of Pharmacology, New York Medical College, Valhalla, NY 10595. E-mail nick_ferreri{at}nymc.edu
Abstract—Tumor necrosis
factor-
(TNF-) and angiotensin II (Ang II) induced a
transient increase in vascular smooth muscle cell (VSMC)
cyclooxygenase-2 (COX-2) mRNA accumulation, without
affecting COX-1 mRNA levels. The kinetics of COX-2 mRNA accumulation
were similar in VSMCs challenged with either TNF- or Ang II; mRNA
accumulation peaked at 2 hours and decreased to control levels by 
6
hours. Accumulation of COX-2 mRNA was associated with a time-dependent
increase of COX-2 protein expression that displayed similar kinetics in
response to either TNF- or Ang II. Both the increase in COX-2 mRNA
accumulation and protein expression in response to either TNF- or
Ang II were inhibited by the mitogen-activated
protein/extracellular signal–regulated kinase (MEK)
inhibitor PD098059. In addition, the
AT1-selective receptor antagonist
losartan attenuated the Ang II–mediated increase in COX-2 mRNA
accumulation; the AT2-selective antagonist
PD123319 had no effect. Prostacyclin I2 synthesis
was tightly coupled to expression of COX-2, whereas
prostaglandin E2 and thromboxane
A2 (TXA2) synthesis may be associated with
differential usage of COX-1 and COX-2. The COX-2–selective
inhibitors NS-398 and nimesulide and the TXA2
receptor antagonist BMS 180,291 inhibited TNF-– and Ang
II–mediated increases in DNA content and cell number by 95%. These
findings suggest that a prostanoid derived from COX-2, possibly
TXA2, may contribute to VSMC hyperplasia in vessel injury
or pathophysiological conditions associated with
elevated levels of either TNF- or Ang II.
Key Words: angiotensin II • tumor necrosis factor- • vascular smooth muscle cells • cyclooxygenase-2
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