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Blood, 15 June 2002, Vol. 99, No. 12, pp. 4443-4448
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Heme oxygenase-1-derived carbon monoxide is an autocrine
inhibitor of vascular smooth muscle cell growth
Kelly J. Peyton,
Sylvia V. Reyna,
Gary B. Chapman,
Diana Ensenat,
Xiao-ming Liu,
Hong Wang,
Andrew I. Schafer, and
William Durante
From the Houston VA Medical Center and the Departments
of Medicine and Pharmacology, Baylor College of Medicine, Houston, TX.
Vascular smooth muscle cells (SMCs) generate carbon monoxide (CO)
via the catabolism of heme by the enzyme heme oxygenase (HO). In the
present study, we found that serum stimulated a time- and
concentration-dependent increase in the levels of HO-1 messenger RNA
(mRNA) and protein in vascular SMCs. The induction of HO-1 expression
by serum was inhibited by actinomycin D or cycloheximide. In addition,
serum stimulated HO activity, as reflected by an increase in the
concentration of bilirubin in the culture media. Treatment of vascular
SMCs with serum stimulated DNA synthesis and this was potentiated by
the HO inhibitors, zinc and tin protoporphyrin-IX as well as by the CO
scavenger, hemoglobin. The iron chelator desferrioxamine had no effect
on DNA synthesis. However, exposure of vascular SMCs to exogenous CO
inhibited serum-stimulated SMC proliferation and the phosphorylation of
retinoblastoma protein. In addition, CO arrested SMCs at the
G1/S transition phase of the cell cycle and selectively
blocked the serum-stimulated expression of cyclin A mRNA and protein
without affecting the expression of cyclin D1 and E. CO also inhibited
the serum-stimulated activation of cyclin A-associated kinase activity
and cyclin-dependent kinase 2 activity. These results demonstrate that
serum stimulates HO-1 gene expression and CO synthesis. Furthermore,
they show that CO acts in a negative feedback fashion to inhibit
vascular SMC growth by regulating specific components of the cell cycle
machinery. The capacity of vascular mitogens to induce CO
synthesis may provide a novel mechanism by which these agents modulate
cell growth.
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