Imbalance between tissue inhibitor of metalloproteinase-4 and matrix metalloproteinases during acute myocardial [correction of myoctardial] XXXX -reperfusion injury.

@entity296 @entity6930 @entity63 @entity34501 @entity741 @entity35 @entity11017
BACKGROUND: We have previously reported that @entity11017 ( @entity11017 ) contributes to @entity741 -reperfusion injury by degradation of troponin I, a regulatory element of the contractile proteins. MMP activities are also tightly regulated by tissue inhibitors of metalloproteinase (TIMPs). The change in TIMPs during acute @entity741 -reperfusion injury is not clear. METHODS AND RESULTS: Isolated @entity35 hearts were perfused either aerobically for 75 minutes or subjected to 15, 20, or 25 minutes of global, no-flow @entity63 followed by 30 minutes of aerobic reperfusion. During reperfusion after @entity63 , there was a rapid, enhanced release of @entity34501 , the most abundant @entity6930 in the heart, into the coronary effluent, as shown both by reverse zymography and Western blot. There was a negative correlation between the recovery of cardiac mechanical function and the release of @entity34501 during reperfusion in hearts subjected to different durations of @entity63 . Immunogold electron microscopy revealed a close association of @entity34501 with the sarcomeres in aerobically perfused hearts. Moreover, @entity34501 was present only in thin myofilaments prepared from aerobically perfused hearts but not in ischemic-reperfused hearts. An enhanced MMP activity was shown in ischemic-reperfused hearts by in situ zymography. CONCLUSIONS: Loss of @entity34501 from the cardiac myocyte leads to an increase in net myocardial MMP activity that contributes to acute @entity296 .
