Regulation of Very-Low-Density Lipoprotein Receptor in Hypertrophic Rat Heart

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...

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Bibliographic Details
Published in:Circulation research 1996-01, Vol.78 (1), p.8-14
Main Authors: Masuzaki, Hiroaki, Jingami, Hisato, Matsuoka, Naoki, Nakagawa, Osamu, Ogawa, Yoshihiro, Mizuno, Megumi, Yoshimasa, Yasunao, Yamamoto, Tokuo, Nakao, Kazuwa
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Cardiology. Vascular system
Cardiomegaly - metabolism
Cells, Cultured
Down-Regulation
Endothelins - pharmacology
Heart
Heart failure, cardiogenic pulmonary edema, cardiac enlargement
Lipoprotein Lipase - metabolism
Lipoproteins, VLDL - metabolism
Medical sciences
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Receptors, LDL - metabolism
RNA, Messenger - analysis
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Summary: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.(Circ Res. 1996;78:8-14.)
ISSN:0009-7330
1524-4571
DOI:10.1161/01.res.78.1.8