Abstract
BackgroundFollowing myocardial infarction (MI), we aimed to characterize morphometric and genetic changes in extracellular matrix (ECM) components from ischemia onset until late phases after coronary reperfusion in necrotic and salvaged myocardium.ResultsSwine were divided into one control (n = 5) and three MI groups: 90-min of ischemia without reperfusion, or followed by 1-week or 1-month reperfusion (n = 5 per group). In samples from the necrotic and salvaged areas, ECM components were morphometrically quantified and mRNA levels of factors involved in ECM remodeling were evaluated. After 90-min of ischemia, fibronectin, laminin, and elastic fibers content as well as upregulated mRNA expression of tissue inhibitors of metalloproteinases (TIMP)1, TIMP2, TIMP3 and connective tissue growth factor increased in the necrotic and salvaged myocardium. In both reperfused MI groups, collagen-I, collagen-III, elastic fibers, glycosaminoglycans, laminin, and fibronectin levels heightened in the necrotic but not the salvaged myocardium. Moreover, mRNA expression of TIMP1, TIMP2 and TIMP3, as well as metalloproteinase-2 and metalloproteinase-9 heightened in the necrotic but not in the salvaged myocardium.ConclusionsMatrix remodeling starts after ischemia onset in both necrotic and salvaged myocardium. Even if ECM composition from the salvaged myocardium was altered after severe ischemia, ECM makes a full recovery to normal composition after reperfusion. Therefore, rapid coronary reperfusion is essential not only to save cardiomyocytes but also to preserve matrix, thus avoiding impaired left ventricular remodeling.
Highlights
Following myocardial infarction (MI), we aimed to characterize morphometric and genetic changes in extracellular matrix (ECM) components from ischemia onset until late phases after coronary reperfusion in necrotic and salvaged myocardium
Percutaneous intervention has played a pivotal role in saving viable cardiomyocytes as well as reducing infarct size and cardiac events [5,6,7], heart failure occurs in post-MI patients, Rios-Navarro et al BMC Veterinary Research (2020) 16:262 mainly due to adverse ventricular geometry and wall thinning [8, 9], and to prevent this, localized and timely regulated ECM remodeling is mandatory after MI [3, 10, 11]
Ninety-min mid-left anterior descending (LAD) coronary artery occlusion was conducted in 20 pigs, three of them died during balloon inflation due to refractory ventricular fibrillation and two during the reperfusion period
Summary
Following myocardial infarction (MI), we aimed to characterize morphometric and genetic changes in extracellular matrix (ECM) components from ischemia onset until late phases after coronary reperfusion in necrotic and salvaged myocardium. The extracellular matrix (ECM) is an imbricated network made up of fibers and ground substance (composed mainly of glycosaminoglycans (GAG), proteoglycans and adhesion glycoproteins). It provides structural support for different cell types, modifies cellular activity and actively participates. Despite the role of ECM after MI has been previously reported [2, 12], we aim to comprehensively examine the morphometric and molecular changes in the ECM occurring in the necrotic and salvaged myocardium from ischemia onset until late phase post-reperfusion. In a swine model of reperfused MI, the specific objectives of this study are: 1) to use morphometric analysis to quantify the presence and organization of ECM components throughout the ischemia-reperfusion process following MI, 2) to compare ECM changes between necrotic and salvaged myocardium, and 3) to pinpoint the dynamics of key genes responsible for ECM remodeling in the necrotic and salvaged myocardium
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