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. Key Words: angiotensin Ⅲ circadian rhythm Ⅲ molecular biology Ⅲ muscle, smooth I n mammals, behavioral and physiological processes display Ϸ24-hour rhythms that are regulated by circadian pacemakers. On the basis of surgical ablation and transplantation experiments, the central circadian pacemaker is thought to reside in the hypothalamic suprachiasmatic nucleus. 1 However, several lines of evidence indicate that peripheral tissues and immortalized cells also contain circadian oscillators; the molecular mechanisms of these oscillators are virtually identical to those in the suprachiasmatic nucleus. [2][3][4][5] The molecular mechanism of this circadian oscillator is based on interacting transcriptional-translational autoregulatory feedback loops. The feedback loop involves 3 homologs of the Drosophila gene period (mPer1, mPer2, and mPer3) and 2 cryptochrome genes (mCry1 and mCry2). The rhythmic transcription of the mPer and mCry genes is driven by the transcription activator genes Clock and Bmal1. 6 Various cardiovascular functions, including blood pressure, heart rate, and coagulation parameters, are known to show a diurnal variation. 7 In addition, several cardiovascular events, such as myocardial infarction, sudden cardiac death, and stroke, show well-defined patterns in their occurrence throughout the day. 8 Although such diurnal variations are widely known, the underlying molecular mechanisms...
ObjectiveTo investigate the no reflow risk factors after percutaneous coronary intervention in ST elevation myocardial infarction patients.MethodSample size, mean ± standard deviation (SD) or frequencies (percent) of normal and no reflow groups were extracted from each study.ResultsOf 27 retrospective and prospective studies, we found that increasing risks of no reflow were associated with advanced age, male, family history of coronary artery disease, smoking, diabetes mellitus, hypertension, delayed reperfusion, killip class ≥2, elevated blood glucose, increased creatinine, elevated creatine kinase (CK), higher heart rate, decreased left ventricular ejection fraction (LVEF), collateral flow ≤1, longer lesion length, multivessel disease, reference luminal diameter, initial thrombolysis in myocardial infarction (TIMI) flow, and high thrombus burden. Moreover, initial TIMI flow ≤1 and high thrombus burden had the greater impact on no reflow (OR95%CI = 3.83 [2.77–5.29], p < 0.0001 and 3.69 [2.39–5.68], p < 0.0001, respectively).ConclusionOur meta-analysis reveals that initial TIMI flow ≤1 and high thrombus burden are the most impacted no reflow risk factors.
NHE3 should represent an output gene of the peripheral oscillators in kidney, which is regulated directly by CLOCK:BMAL1 heterodimers.
Background: Individually, green tea and green coffee have been extensively studied for mitigation of metabolic syndrome (MS) in both rats and humans; however, their combined effect requires further investigation. Thus, we compared the metabolic effect of combining green tea and decaffeinated light roasted green coffee on MS in rats. Methods: An MS animal model was constructed by feeding Sprague-Dawley rats with a high-fat-high-sucrose (HFHS) diet for eight weeks and a low dose of streptozotocin (STZ) injection at week 2. Rats fed with HFHS diets and injected with STZ successfully developed MS phenotypes, indicated by higher body weight, systolic blood pressure, plasma triglyceride level, plasma fasting blood glucose level, and lower plasma HDL-C level, compared to those fed with a normal chow diet. Subsequently, MS rats were continuously fed with HFHS and divided into four groups: MS rats, MS with 300 mg/bw.t green tea extract (GT), MS with 200 mg/bw.t green coffee extract (GC), and MS with combined green tea and green coffee extract (CM) for nine weeks. Results: Combining green tea and green coffee have synergistic effects on reducing plasma fasting blood glucose and triglyceride level. Inflammatory markers both in plasma and liver tissue robustly decreased in CM group rats. However, the reduction of systolic blood pressure was observed only in GT and CM groups. Moreover, all treatment resulted in an increase in plasma HDL-C level in MS rats. Conclusions: Our data highlighted that, in MS animal models, combined green tea and decaffeinated light roasted green coffee augment their several individual beneficial effects of improved metabolic parameters and modulated inflammatory genes.
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