Regulation of very-low-density lipoprotein receptor in hypertrophic rat heart
Regulation of very-low-density lipoprotein receptor in hypertrophic rat heart
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DOI：
10.1161/01.res.78.1.8
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发表时间：
1996-01-01
影响因子：
20.1
通讯作者：
Nakao, K
中科院分区：
文献类型：
--
作者：
Masuzaki, H;Jingami, H;Nakao, K
为了阐明极低密度脂蛋白（VLDL）受体的调节，我们研究了其基因表达在自发性高血压大鼠中风倾向（SHR-SP，高血压诱导的心脏肥大的动物模型）与Wistar-Kyoto大鼠相比。RNA酶保护试验表明，心室VLDL受体mRNA福尔斯在4周时下降到正常水平的41%，此时高血压尚未完全发展，并在13周时进一步下降到14%，此时心脏肥大已经建立。脂蛋白脂酶mRNA与VLDL受体mRNA平行降低。10（-8）mol/L内皮素-1处理乳鼠心室肌细胞24小时后，VLDL受体mRNA水平下降，仅为初始值的40%，与心肌细胞肥大的进程相一致。这些结果表明，在体内和体外的心脏肥大的VLDL受体基因表达下调，并表明，VLDL受体的调节可能与开关的能量底物从脂质到葡萄糖已知发生在心脏肥大。
To elucidate the regulation of very-low-density lipoprotein (VLDL) receptor, we have studied its gene expression in the heart of spontaneously hypertensive rats-stroke prone (SHR-SP, an animal model for hypertension-induced cardiac hypertrophy) compared with Wistar-Kyoto rats. RNase protection assay showed that ventricular VLDL receptor mRNA falls to 41% of normal levels at 4 weeks, when hypertension is not yet fully developed, and drops further to 14% at 13 weeks, when cardiac hypertrophy is established. Lipoprotein lipase mRNA decreases in parallel with VLDL receptor mRNA. In cultured neonatal rat ventricular cardiomyocytes, VLDL receptor mRNA decreases in parallel with the process of cardiocyte hypertrophy during the 24 hours after treatment with 10(-8) mol/L endothelin-1, falling to 40% of the initial value. These results demonstrate that there is downregulation of VLDL receptor gene expression in cardiac hypertrophy both in vivo and in vitro and suggest that the regulation of the VLDL receptor is possibly linked with the switch in energy substrate from lipid to glucose known to occur in cardiac hypertrophy.