Circulation, Vol 84, 1266-1272, Copyright © 1991 by American Heart Association
GK Hansson and J Holm
BACKGROUND. Arterial injury initiates a proliferative response among the
smooth muscle cells of the artery. This leads to the formation of a
thickened intima that may reduce the diameter of the arterial lumen. Such
intimal lesions often develop after vascular surgery and angioplastic
procedures. Previous cell culture studies have shown that the lymphokine,
interferon-gamma (gIFN), inhibits smooth muscle cell proliferation. METHODS
AND RESULTS. We therefore tested whether administration of exogenous gIFN
could inhibit the development of intimal lesions. Rat carotid arteries were
denuded with a balloon catheter, resulting in the formation of a
standardized intimal lesion. The animals were then treated with recombinant
rat gIFN at 200,000 units (approximately 400,000 units or 100 micrograms/kg
body wt) administered parenterally once daily for 7 days. Autoradiographic
analysis of 3H-thymidine incorporation revealed that gIFN reduced the early
smooth muscle replication by approximately 75%. gIFN treatment for 1 week
resulted in a 50% reduction of intimal cross-section area at 2 weeks after
injury when compared to control rats injected with buffer alone. The
difference in lesion development persisted in rats analyzed 10 weeks after
injury, suggesting that proliferative events during the first week
determine the long-term development of the intima. Inhibition of lesion
development was accompanied by expression of the class II
histocompatibility (Ia) gene, RT1B, suggesting that both were directly
related to the administration of gIFN. CONCLUSIONS. These results show that
gIFN is a potent inhibitor of the formation of arterial proliferative
lesions in vivo. It is possible that gIFN could be useful in preventing
arterial stenosis after surgery and angioplasty in man.
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Interferon-gamma inhibits arterial stenosis after injury
Department of Clinical Chemistry, Gothenburg University, Sweden.
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