© 1998 American Heart Association, Inc.
Original Contributions |
Expression of Extracellular Matrix Proteins Accompanies Lesion Growth in a Model of Intimal Reinjury
From the Department of Pathology, University of Washington, Seattle.
Abstract—Reinjury of rat
arterial lesions induces an increase in lesion size that is
not associated with an increase in cell number. In this study, matrix
volume was examined after reinjury to preexisting lesions, and the
kinetics of matrix gene expression and activity of proteolytic enzymes
in the lesion were evaluated. Volume densitometry in intima showed a
significant increase in matrix volume 28 days after the reinjury,
although no change was observed at 14 days. Three common vascular
matrix molecules, 
1(I)procollagen, tropoelastin, and
fibronectin, were expressed highly at 7 days after the reinjury.
Expression of tropoelastin remained upregulated for the entire 28 days
after the reinjury, whereas 1(I)procollagen and
fibronectin returned to the control level by 28 days. Protease activity
was also increased after reinjury. Within days, a marked increase in
urokinase plasminogen activator activity was
observed in intima, and this activity decreased to control level by 14
days. The activity of tissue plasminogen
activator did not change. The 95-kDa
gelatinolytic activity was increased 1 to 2 days
after the reinjury, but no change in other
gelatinolytic activities was observed. These
findings demonstrate that the accumulation of extracellular matrix is
important in the increase in lesion size after reinjury and that a
balance of matrix synthesis and degradation may explain why no change
in matrix volume was detected until 28 days after the reinjury.
Key Words: angioplasty • extracellular matrix • plasminogen activator • matrix metalloproteinase
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