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and myocardial matrix metalloproteinases in heart
failure: relationship to LV remodeling
1 Medical University of South Carolina, Charleston, South Carolina 29425; and 2 St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada M5B 1W8
The cytokine tumor
necrosis factor (TNF)-
has been causally linked to left
ventricular (LV) remodeling, but the molecular basis for this
effect is unknown. Matrix metalloproteinases (MMPs) have been
implicated in cardiac remodeling and can be regulated by TNF-. This
study tested the central hypothesis that administration of a TNF-
blocking protein would prevent the induction of MMPs and alter the
course of myocardial remodeling in developing LV failure. Adult dogs
were randomly assigned to the following groups: 1) chronic
pacing (250 beats/min, 28 days, n = 12), 2)
chronic pacing with concomitant administration of a TNF- blocking
protein (TNF block) using a soluble p75 TNF receptor fusion protein
(TNFR:Fc; administered at 0.5 mg/kg twice a week subcutaneously,
n = 7), and 3) normal controls
(n = 10). LV end-diastolic volume increased from
control with chronic pacing (83 ± 12 vs. 118 ± 10 ml,
P < 0.05) and was reduced with TNF block (97 ± 9 ml, P < 0.05). MMP zymographic levels (92 kDa, pixels)
increased from control with chronic pacing (36,848 ± 9,593 vs.
87,247 ± 12,912, P < 0.05) and was normalized by
TNF block. Myocardial MMP-9 and MMP-13 levels by immunoblot increased
with chronic pacing relative to controls (130 ± 10% and 118 ± 6%, P < 0.05) and was normalized by TNF block. These results provide evidence to suggest that TNF- contributes to
the myocardial remodeling process in evolving heart failure through the
local induction of specific MMPs.
tumor necrosis factor-; chronic pacing
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