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Volume 272, Number 52, Issue of December 26, 1997
pp. 32804-32809
(Received for publication, August 25, 1997, and in revised form, October 16, 1997)
From the Excess vascular smooth muscle cell (VSMC)
proliferation and contractility are key events in the pathophysiology
of vascular disorders induced by hypoxia. We have recently reported
that carbon monoxide (CO), produced by VSMC under conditions of
hypoxia, can be a modulator of cGMP levels in both endothelial and
smooth muscle cells. In this respect, some of the physiologic effects
of CO in the vasculature parallel those of nitric oxide (NO), a well characterized regulator of vascular tone. We report here that under
hypoxia, VSMC-derived CO is an important regulator of VSMC proliferation. Inhibiting CO formation or scavenging CO with hemoglobin increased VSMC proliferation in response to serum or to mitogens such
as endothelin, whereas increasing CO production or exposing cells to
exogenous CO lead to a markedly attenuated growth response. The effects
of CO on VSMC proliferation correlated with changes in E2F-1
expression, the prototype member of a family of transcription factors
that participate in the control of cell cycle progression. CO
significantly suppressed E2F-1 expression, whereas, removal of CO from
the cultures with hemoglobin lead to increased E2F-1 gene
transcription, mRNA, and protein production as well as mRNA levels of c-myc, a target gene of E2F-1. Moreover, the
actions of CO were mediated by the second messenger molecule, cGMP.
Limiting VSMC growth by increasing the release of CO may represent a
key event in the body's compensatory responses to hypoxia.
Carbon Monoxide Controls the Proliferation of Hypoxic Vascular
Smooth Muscle Cells
,
,
and
Joint Program in Neonatology, Department of
Pediatrics, Harvard Medical School, Boston, Massachusetts 02115 and the
§ Department of Medicine, Boston University Medical Center,
Boston, Massachusetts 02118
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