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Volume 4, Issue 3, Pages 227-234 (September 1997) Dynamic extracellular matrix remodeling in the heart failure: cardiac hypertrophy, dilatation and fibrosis Suresh C Tyagi Pathophysiology Volume 4, Issue 3, Pages 227-234 (September 1997) DOI: 10.1016/S0928-4680(97)00019-9

Fig. 1 Hypertrophy in the non-infarcted heart and thin wall in the infarcted heart. In the ischemic heart some parts are hypertrophic whereas other parts have a very thin heart wall. This figure shows an explanted human heart with ischemic cardiomyopathy. Infarction is apparent by discoloration and the thin wall. The tissue is very soft at the site of infarction in comparison to the non-infarcted heart. The normal heart is smaller in size than the ischemic heart. The cross section of the ischemic heart demonstrates thin walls and infarction, as well as thick hypertrophic walls and non-infarction in the same heart. This suggests a differential structural remodeling in the ischemic heart following heart failure. LV, left ventricle; RV, right ventricle; Gel, gelatinase; Int col, interstitial collagenase. Pathophysiology 1997 4, 227-234DOI: (10.1016/S0928-4680(97)00019-9)

Fig. 2 Differential localization of MMP in the infarcted and non-infarcted ischemic heart. Pathophysiology 1997 4, 227-234DOI: (10.1016/S0928-4680(97)00019-9)

Fig. 3 Differential expression of gelatinase activity in normal, non-infarcted and infarcted hearts. The total collagenase/gelatinase activity was measured by zymography [24]. The gels were scanned to measure the lytic intensity. In the endo- and epimyocardium of infarcted LV, collagenase activity was 85–95 and 10–20%, respectively, compared with only 5–10 and 3–5%, respectively, in noninfarcted LV, with respect to the total 100% (active and latent) collagenase. In the normal heart we found 3±1% collagenase activity which could be activated to 80–90% by trypsin or plasmin, indicating that collagenase is normally inactive and/or in a latent form in the normal heart [20, 21]. Zymographic (A, lane 1) and immuno-blot analysis demonstrated the presence of one band at 66 kDa (MMP-2) in the normal tissue. Normal tissue was obtained from post-transplant endomyocardial biopsies. However, expression of 66 kD band in the non-infarcted heart (A, lanes 2, 3) was increased significantly (P<0.01) as compared with the normal heart. Under these conditions, an identical amount of total protein was loaded onto the gel (SDS-PAGE, B). In the infarcted heart we observed several lytic bands at 92 (gelatinase B), 66 (gelatinase A) and 54 kDa (MMP-1) in gelatin zymography [19](A, lane 4). The higher molecular weight gelatinases are non-specific binding gelatinases as discussed [19]. These results suggested that MMPs are regulated differentially in the infarcted, non-infarcted and normal heart. Pathophysiology 1997 4, 227-234DOI: (10.1016/S0928-4680(97)00019-9)

Fig. 4 Schematic presentation of early, compensatory and late proteolytic cascade following ischemic injury at the site of infarction and non-infarction. Pathophysiology 1997 4, 227-234DOI: (10.1016/S0928-4680(97)00019-9)

Fig. 5 Cellular response of the expression of proteolytic cascade during ischemic cardiomyopathy. Pathophysiology 1997 4, 227-234DOI: (10.1016/S0928-4680(97)00019-9)

Fig. 6 Ischemia induces transendothelial neutrophil migration into the interstitium. Neutrophil proteinasess and oxidants released during migration degrade basement membrane and elastic laminal components. Pathophysiology 1997 4, 227-234DOI: (10.1016/S0928-4680(97)00019-9)