(Circulation. 2000;102:1697.)
© 2000 American Heart Association, Inc.
Basic Science Reports |
Direct Evidence for Cytokine Involvement in Neointimal Hyperplasia
From the University of Florida College of Medicine, Malcom Randall VAMC, Gainesville, Fla.
Correspondence to C. Keith Ozaki, MD, PO Box 100286, Gainesville, FL 32610. E-mail ozaki{at}surgery.ufl.edu
Background—Tumor necrosis
factor-
(TNF-) and interleukin 1 (IL-1) are proximal inflammatory
cytokines that stimulate expression of adhesion molecules and
induce synthesis of other proinflammatory cytokines. In
addition, TNF- and IL-1 influence vascular smooth muscle cell
migration and proliferation in vitro. In view of the inflammatory
nature of neointimal hyperplasia (NIH), we tested the
hypothesis that endogenous TNF- and IL-1 modulate low
shear stress–induced NIH.
Methods and Results—Mice underwent unilateral common carotid
artery (CCA) ligation. Low shear stress in the patent ligated CCA has
previously been shown to result in remodeling and NIH. Reverse
transcriptase–polymerase chain reaction for TNF- and IL-1 mRNA
demonstrated both TNF- and IL-1 mRNA in ligated CCAs, whereas
normal and sham-operated CCAs had none. Mice lacking functional TNF-
(TNF-/-) developed 14-fold less neointimal area than WT
controls (P<0.05). p80 IL-1 type I receptor knockout
(IL-1RI-/-) mice tended to develop less (7-fold,
P>0.05) neointimal area than WT controls.
Furthermore, no IL-1 mRNA expression was detected in CCAs from
TNF-/- mice; however, TNF- mRNA expression was found in the
IL-1RI-/- mice. Mice that overexpress membrane-bound TNF- but
produce no soluble TNF- display an accentuated fibroproliferative
response to low shear stress (P<0.05).
Conclusions—These results directly demonstrate that TNF- and
IL-1 modulate NIH induced by low shear stress. NIH can proceed by way
of soluble TNF-–independent mechanisms. Specific anti–TNF- and
anti–IL-1 therapies may lessen NIH.
Key Words: remodeling • restenosis • atherosclerosis • carotid arteries
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