Faculty of Pharmacy, Université de Montréal, Montreal, Quebec, Canada.
Department of Chemistry, Université de Montréal, Montreal, Quebec, Canada.
FASEB J. 2018 Feb;32(2):807-818. doi: 10.1096/fj.201700505R. Epub 2018 Jan 4.
CD36 is a multiligand receptor involved in lipid metabolism. We investigated the mechanisms underlying the cardioprotective effect of CP-3(iv), an azapeptide belonging to a new class of selective CD36 ligands. The role of CP-3(iv) in mediating cardioprotection was investigated because CD36 signaling leads to activation of peroxisome proliferator-activated receptor-γ, a transcriptional regulator of adiponectin. CP-3(iv) pretreatment reduced infarct size by 54% and preserved hemodynamics in C57BL/6 mice subjected to 30 min coronary ligation and reperfusion but had no effect in CD36-deficient mice. The effects of CP-3(iv) were associated with an increase in circulating adiponectin levels, epididymal fat adiponectin gene expression, and adiponectin transcriptional regulators ( Pparg, Cebpb, Sirt1) after 6 h of reperfusion. Reduced myocardial oxidative stress and apoptosis were observed along with an increase in expression of myocardial adiponectin target proteins, including cyclooxygenase-2, phospho-AMPK, and phospho-Akt. Moreover, CP-3(iv) increased myocardial performance in isolated hearts, whereas blockade of adiponectin with an anti-adiponectin antibody abrogated it. CP-3(iv) exerts cardioprotection against myocardial ischemia and reperfusion (MI/R) injury and dysfunction, at least in part, by increasing circulating and myocardial adiponectin levels. Hence, both paracrine and endocrine effects of adiponectin may contribute to reduced reactive oxygen species generation and apoptosis after MI/R, in a CD36-dependent manner.-Huynh, D. N., Bessi, V. L., Ménard, L., Piquereau, J., Proulx, C., Febbraio, M., Lubell, W. D., Carpentier, A. C., Burelle, Y., Ong, H., Marleau, S. Adiponectin has a pivotal role in the cardioprotective effect of CP-3(iv), a selective CD36 azapeptide ligand, after transient coronary artery occlusion in mice.
CD36 是一种多配体受体,参与脂质代谢。我们研究了 CP-3(iv)的心脏保护作用的机制,CP-3(iv) 是一种属于新型选择性 CD36 配体的氮杂肽。CP-3(iv) 介导心脏保护作用的作用是因为 CD36 信号导致过氧化物酶体增殖物激活受体-γ(脂联素的转录调节剂)的激活。CP-3(iv) 预处理可使 C57BL/6 小鼠在 30 分钟冠状动脉结扎和再灌注后梗死面积减少 54%,并保持血液动力学,但在 CD36 缺陷型小鼠中没有作用。CP-3(iv) 的作用与循环脂联素水平的升高、附睾脂肪脂联素基因表达和脂联素转录调节剂(Pparg、Cebpb、Sirt1)有关在再灌注 6 小时后。观察到心肌氧化应激和凋亡减少,同时表达心肌脂联素靶蛋白增加,包括环氧化酶-2、磷酸化-AMPK 和磷酸化-Akt。此外,CP-3(iv) 增加了离体心脏的心肌性能,而用抗脂联素抗体阻断脂联素则消除了它。CP-3(iv) 对心肌缺血再灌注(MI/R)损伤和功能障碍具有心脏保护作用,至少部分是通过增加循环和心肌脂联素水平。因此,脂联素的旁分泌和内分泌作用可能有助于减少 MI/R 后活性氧的产生和细胞凋亡,这是一种依赖于 CD36 的方式。-Huynh, D. N.、Bessi, V. L.、Ménard, L.、Piquereau, J.、Proulx, C.、Febbraio, M.、Lubell, W. D.、Carpentier, A. C.、Burelle, Y.、Ong, H.、Marleau, S. 脂联素在 CP-3(iv)(一种新型选择性 CD36 氮杂肽配体)后短暂性冠状动脉闭塞对小鼠的心脏保护作用中起关键作用。