Angiotensin II induces circadian gene expression of clock genes in cultured vascular smooth muscle cells
| Autor: | Sunu Budhi Raharjo, Hidemi Nonaka, Mitsuhiro Yokoyama, Hitoshi Okamura, Hiroyuki Fukuya, Mohammad Saifur Rohman, Koji Ikeda, Noriaki Emoto, Kazuhiro Yagita |
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| Rok vydání: | 2001 |
| Předmět: |
Male
medicine.medical_specialty Vascular smooth muscle Pyridines Gene Expression Tetrazoles Aorta Thoracic Cell Cycle Proteins Biology RAR-related orphan receptor alpha Receptor Angiotensin Type 2 Muscle Smooth Vascular Receptor Angiotensin Type 1 Angiotensin Receptor Antagonists Mice Biological Clocks Physiology (medical) Internal medicine medicine Basic Helix-Loop-Helix Transcription Factors Animals Circadian rhythm Northern blot RNA Messenger Cells Cultured Mice Inbred BALB C Suprachiasmatic nucleus Angiotensin II Biphenyl Compounds Imidazoles ARNTL Transcription Factors Nuclear Proteins Period Circadian Proteins Blotting Northern Circadian Rhythm Rats CLOCK DNA-Binding Proteins Endocrinology Benzimidazoles Cardiology and Cardiovascular Medicine Biomarkers Transcription Factors |
| Zdroj: | Circulation. 104(15) |
| ISSN: | 1524-4539 |
| Popis: | Background Daily rhythms of mammalian physiology and endocrinology are regulated by circadian pacemakers. The master circadian pacemaker resides in the suprachiasmatic nucleus, which is located in the hypothalamus of the brain, but circadian oscillators also exist in peripheral tissues. Because many studies have demonstrated apparent circadian variations in the frequency of cardiovascular disorders, it is of great interest to investigate a possible relation between circadian gene expression and cardiovascular function. We examined whether a circadian oscillation system exists in the aorta and/or in cultured vascular smooth muscle cells (VSMCs). Methods and Results The mRNA levels of clock genes were assayed by northern blot analysis. The mouse aorta showed a clear circadian oscillation in the expression of mPer2 , dbp , and Bmal1 . Brief treatment of VSMCs with angiotensin II induced a robust increase in mPer2 gene expression, followed by a marked reduction in mPer2 mRNA levels and subsequent synchronous cycling of mPer2 , dbp , and Bmal1 mRNAs. The induction of mPer2 in VSMCs by angiotensin II was completely abolished by treatment with CV11947, a specific angiotensin II type1 receptor antagonist. Conclusions The present results demonstrate that the aorta and VSMCs possess a circadian oscillation system which is comparable to that of the suprachiasmatic nucleus and that the circadian gene expression in VSMCs is induced by angiotensin II through the angiotensin II type1 receptor. Our in vitro system will provide a useful tool to further analyze the physiological significance of the peripheral clock in cardiovascular function. |
| Databáze: | OpenAIRE |
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