Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:490-497
© 1997 American Heart Association, Inc.
Articles |
Tumor Necrosis Factor-
Activates Smooth Muscle Cell Migration in Culture and Is Expressed in the Balloon-Injured Rat Aorta
From the King Gustaf V Research Institute, Karolinska Hospital (S.J., J.R., J.N.), and the Department of Cell and Molecular Biology, Division of Cell Biology, Karolinska Institute (A.H.N.), Stockholm, Sweden.
Correspondence to Dr Stefan Jovinge, King Gustaf V Research Institute, Karolinska Hospital, S-171 76 Stockholm, Sweden. E-mail jovinge{at}instmed.ks.se.
Abstract In experimental models of atherosclerosis,
activation of smooth muscle cell (SMC) migration from the media to the
intima is preceded by intimal accumulation of inflammatory cells,
suggesting that cytokines may be involved in this process. The present
study demonstrates that tumor necrosis factor- (TNF-) regulates
cytoskeletal organization of SMCs by inducing depolymerization of actin
stress fibers and dispersion of vinculin from sites of focal adhesion
and stimulates the migration of cultured human SMCs in a dose-dependent
manner. Moreover, TNF- induces rapid activation of the
c-ets-1 gene, which codes a transcription factor known to
regulate enzymes important for matrix degradation during cell
migration. Balloon catheter injury of the rat femoral artery resulted
in medial expression of TNF- within 6 hours. This expression
appeared to be localized to SMCs and remained elevated until SMCs began
to migrate into the intima 7 days after injury. These findings
demonstrate that TNF- has a stimulatory effect on SMC
migration and suggest that TNF- may be involved in the intimal
recruitment of SMCs during plaque formation.
Key Words: tumor necrosis factor- • smooth muscle cells • migration • ets-1
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