Key result
MI in rats increases lipoprotein receptor expression and drives ~30% greater LDE uptake versus sham.
In a rat model of myocardial infarction, lipoprotein receptor expression is increased in the infarcted area, suggesting a potential mechanism involved in myocardial repair and left ventricular remodeling.
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Animal data suggest LDL receptors may contribute to post-MI remodeling; leaves open human relevance and therapeutic targeting.
Left ventricular (LV) remodeling after myocardial infarction constitutes the structural basis for ventricular dysfunction and heart failure. The characterization underlying the expression of lipoprotein receptors in cardiac dysfunction is scarcely explored. The aim of this study was to analyze the status of lipoprotein receptors on the infarcted and noninfarcted areas of LV and to verify whether nanoparticles that mimic the lipid structure of low-density lipoprotein (LDL) and have the ability to bind to LDL receptors (LDE) are taken up more avidly by the noninfarcted LV. 13 male Wistar rats with left coronary artery ligation (myocardial infarction [MI]) and 12 animals with SHAM operation (SHAM) were used in this study. 6 weeks after the procedure, the quantification of low-density lipoprotein receptor (LDLR), LDL receptor-related protein 1 (LRP1), scavenger receptor-class B type I (SR-BI) lipoprotein receptors, and PCNA proliferation marker, and tissue uptake of radioactively labeled LDE were performed. Immunohistochemistry and Western blot analysis showed that LDLR, LRP1, SR-BI, and PCNA, expression in infarcted area of MI was remarkably higher than SHAM and noninfarcted subendocardial (SEN) and interstitial (INT) areas. In addition, in SEN noninfarcted area of MI, the presence of LDLR was about threefold higher than in SHAM SEN and INT noninfarcted areas. The LDE uptake of noninfarcted LV of MI group was about 30% greater than that of SHAM group. In conclusion, these findings regarding the status of lipoprotein receptors after MI induction could help to establish mechanisms on myocardial repairing. In conclusion, infarcted rats with LV dysfunction showed increased expression of lipoprotein receptors mainly in the infarcted area.
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Lima et al. (2018) studied Myocardial infarction (n=25). Left coronary artery ligation vs. SHAM operation was evaluated on Expression of lipoprotein receptors (LDLR, LRP1, SR-BI), PCNA proliferation marker, and tissue uptake of LDE. Myocardial infarction in rats increased lipoprotein receptor expression in the infarcted area and resulted in ~30% greater LDE uptake in the noninfarcted left ventricle compared to SHAM.
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