Effects of aging and subsequent exercise training on gene expression of endothelin-1 in rat heart

2002 ◽  
Vol 103 (s2002) ◽  
pp. 152S-157S ◽  
Author(s):  
Motoyuki IEMITSU ◽  
Takashi MIYAUCHI ◽  
Seiji MAEDA ◽  
Takumi TANABE ◽  
Yoko IRUKAYAMA-TOMOBE ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Mrna Expression ◽  
Natriuretic Peptide ◽  
Young Group ◽  
Aged Rats ◽  
Aged Group ◽  
Endothelin 1 ◽  
Rat Hearts

Endothelin-1 (ET-1) is produced by endothelial cells and cardiac myocytes. ET-1 has potent positive inotropic and chronotropic effects on heart and induces myocardial cell hypertrophy. We investigated whether gene expression of ET-1 in rat hearts is altered by aging and subsequent exercise training. We also investigated whether gene expression of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), which participate in some pathological cardiac conditions, in the rat hearts is altered by aging and subsequent exercise training. We studied mRNA expression of ET-1, ANP and BNP in hearts of sedentary young rats (Sedentary young; 4 months old), sedentary aged rats (Sedentary aged; 23 months old), and swim-trained aged rats (Trained aged; 23 months old, swimming training for 8 weeks). The left ventricle weight mass index for body weight and left ventricular end-diastolic dimension were significantly higher in the Trained aged group compared with the Sedentary aged group. These results showed that Trained aged rats developed cardiac hypertrophy with improvement of cardiac function. The mRNA expression of ET-1 in the heart was significantly higher in Sedentary aged group compared with Sedentary young group, and was significantly higher in the Trained aged group compared with the Sedentary aged group. The mRNA expression of ANP and BNP in the heart was significantly higher in Sedentary aged group compared with Sedentary young group, and was significantly higher in the Trained aged group compared with the Sedentary aged group. The present results show that mRNA expression of ET-1 in the heart is increased by aging, and that the mRNA expression is further increased by exercise-induced cardiac hypertrophy, suggesting that ET-1 in the heart may participate in these physiological cardiac adaptations.

Effects of exercise training on expression of endothelin-1 mRNA in the aorta of aged rats

2002 ◽  
Vol 103 (s2002) ◽  
pp. 118S-123S ◽  
Author(s):  
Seiji MAEDA ◽  
Takashi MIYAUCHI ◽  
Motoyuki IEMITSU ◽  
Takumi TANABE ◽  
Tomoko YOKOTA ◽  
...  
Keyword(s):  
Exercise Training ◽  
Endothelial Function ◽  
Vascular Endothelial Cells ◽  
Young Group ◽  
Aged Rats ◽  
Aged Group ◽  
Endothelin 1 ◽  
Real Time Quantitative Pcr ◽  
Vascular Tonus ◽  
Potent Vasoconstrictor

Aging impairs endothelial function and the vascular tone regulation, although the precise mechanism remains unclear. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide produced by vascular endothelial cells. Because ET-1 has a potent vasoconstrictor effect on vessels, it may be involved in the regulation of vascular tonus. We hypothesized that aging causes a decrease in ET-1 expression in aorta, and that exercise training improves the aging-induced decrease in ET-1 expression in aorta. This study was performed to examine whether gene expression of ET-1 in the aorta of rats is altered by aging and subsequent exercise training. We studied expression of ET-1 mRNA in the aortas of sedentary young rats (Sedentary young group, 4 months old), sedentary aged rats (Sedentary aged group, 23 months old), and swim trained aged rats (Training aged group, 23 months old; swimming training for 8 weeks, 5days/week, 90min/day). The expression of ET-1 mRNA in the aorta was analysed by real-time quantitative PCR. Body weight and resting heart rate were significantly lower in the Training aged group compared with the Sedentary aged group. These results suggest that the Training aged rats exhibited physiological effects from exercise training. The expression of ET-1 mRNA in the aorta was markedly lower in Sedentary aged group compared with the Sedentary young group, whereas it was significantly higher in Training aged group compared with the Sedentary aged group. These results show that the expression of ET-1 mRNA in the aorta is decreased by aging, and that the expression is increased by exercise training. Therefore, the present study provides a possibility that exercise training improves endothelial function through up-regulation of the aging-induced decrease in ET-1 expression in the aorta.

Muscle microvascular adaptation and angiogenic gene induction in response to exercise training are attenuated in middle-aged rats

2015 ◽  
Vol 11 (1) ◽  
pp. 23-33
Author(s):  
J. Suzuki
Keyword(s):  
Exercise Training ◽  
Acute Exercise ◽  
Young Group ◽  
Treadmill Running ◽  
Mrna Levels ◽  
Aged Rats ◽  
Middle Aged ◽  
Vegf Mrna ◽  
Aged Group ◽  
Exercise Induced

This study was designed to investigate exercise-induced changes in muscle capillarisation, the mRNA expression of angiogenic genes, and microRNA levels in young and middle-aged rats. Rats in the training groups were subjected to treadmill running 5 days a week for 3 weeks. The exercise protocol for the young (12-week old) group was 20-25 m/min, 40-60 min/day with a gradient of 15%, and for the middle-aged (12-month old) group was 18-20 m/min, 40-60 min/day with a gradient of 5%. The enzyme histochemical identification of capillary profiles was performed on cross-sections of gastrocnemius muscle. Total RNA was isolated, reverse transcription was performed, and mRNA and microRNA levels were determined by real-time PCR. The capillary-to-fibre ratio was significantly increased by exercise training in the young group (by 10%), but only slightly in the middle-aged (by 5%) group. Vascular endothecial growth factor (VEGF) mRNA levels were at significantly higher values after acute exercise (1.6-fold) and the 3-week training protocol (1.9-fold) in the young group, but not in the middle-aged group. VEGF protein expression levels were significantly increased after training in the young group only. Endothelial nitric oxide synthase, VEGF-R2 and thrombospondin-1 mRNA levels were significantly lower in the middle-aged group than in the young group. Anti-angiogenic miR-195 levels were significantly enhanced by exercise training in the middle-aged group only. These results indicated that the exercise-induced adaptation of muscle capillarity was attenuated in middle-aged rats, possibly by the lower induction of VEGF and up-regulation of anti-angiogenic miRNA expression.

Alteration of Atrial Natriuretic Peptide and Brain Natriuretic Peptide Gene Expression Associated with Progression and Regression of Cardiac Hypertrophy in Renovascular Hypertensive Rats

1996 ◽  
Vol 90 (3) ◽  
pp. 197-204 ◽  
Author(s):  
Hideo Kawakami ◽  
Hideki Okayama ◽  
Mareomi Hamada ◽  
Kunio Hiwada
Keyword(s):  
Gene Expression ◽  
Atrial Natriuretic Peptide ◽  
Cardiac Hypertrophy ◽  
Brain Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Mrna Levels ◽  
Hypertensive Rats ◽  
Regression Of Cardiac Hypertrophy ◽  
Peptide Gene ◽  
Atrial Natriuretic

1. We assessed the changes of atrial natriuretic peptide and brain natriuretic peptide gene expression associated with progression and regression of cardiac hypertrophy in renovascular hypertensive rats (RHR). 2. Two-kidney, one-clip hypertensive rats (6-week-old male Wistar) were made and studied 6 (RHR-1) and 10 weeks (RHR-2) after the procedure. Regression of cardiac hypertrophy was induced by nephrectomy at 6 weeks after constriction, and the nephrectomized rats were maintained further for 4 weeks (nephrectomized rat: NEP). Sham operation was performed, and the rats were studied after 6 (Sham-1) and 10 weeks (Sham-2). Atrial natriuretic peptide and brain natriuretic peptide gene expression in the left ventricle was analysed by Northern blotting. 3. Plasma atrial natriuretic peptide and brain natriuretic peptide were significantly higher in RHR-1 and RHR-2 than in Sham-1, Sham-2 and NEP. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels in RHR-1 were approximately 7.2-fold and 1.8-fold higher than those in Sham-1, respectively, and the corresponding levels in RHR-2 were 13.0-fold and 2.4-fold higher than those in Sham-2, respectively. Atrial natriuretic peptide and brain natriuretic peptide mRNA levels of NEP were normalized. Levels of atrial natriuretic peptide and brain natriuretic peptide mRNA were well correlated positively with left ventricular weight/body weight ratios. There was a significant positive correlation between the levels of atrial natriuretic peptide and brain natriuretic peptide mRNA (r = 0.86, P<0.01). 4. We conclude that the expression of atrial natriuretic peptide and brain natriuretic peptide genes is regulated in accordance with the degree of myocardial hypertrophy and that the augmented expression of these two natriuretic peptides may play an important role in the maintenance of cardiovascular haemodynamics in renovascular hypertension.

P3486Experimental model for heart failure in rats: apelin-13/apj and bnp-45 gene expression analysis

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H R Helmi ◽  
A P Sunjaya ◽  
D Limanan ◽  
A R Prijanti ◽  
S W A Jusman ◽  
...  
Keyword(s):  
Gene Expression ◽  
Heart Failure ◽  
Cardiac Hypertrophy ◽  
Mrna Expression ◽  
Rat Model ◽  
Control Group ◽  
P Value ◽  
Sprague Dawley ◽  
Hypoxia Exposure ◽  
Systemic Hypoxia

Abstract Background Apelin, an adipokine peptide and its receptor has recently emerged as a key signaling pathway in maintaining cardiac performance at chronic pressure loads. Apelin has been linked to ventricular dysfunction and therefore maybe of pathophysiologic relevance as a candidate biomarker in HF patients. Purpose This study aims to investigate Apelin-13 gene expression and level, and Apelin receptor (APJ) level in a rat model of heart failure induced by chronic systemic hypoxia and their correlation to BNP-45 gene expression and level, the current gold standard biomarker for heart failure, and to cardiac histopathologic changes. The effect of chronic systemic hypoxia on cardiac hypertrophy, remodeling and heart failure parameters is also of interest. Methods Twenty-eight male Sprague-Dawley rats (8–12 weeks of age) were placed in special hypoxic chambers divided into 7 groups – a control group provided with normoxia (atmospheric O2 levels) and 6 exposure groups exposed to hypoxia (8% O2) for 6 hours, 1, 3, 5, 7 and 14 days respectively prior to measurement. Changes in the expression of Apelin and BNP-45 were measured using quantitative real-time PCR, whereas changes in Apelin-13, APJ and BNP-45 levels were measured using ELISA. Histopathology staining using Hematoxylin and Eosin was performed on cardiac tissues post-termination. Results Compared to control, BNP-45 mRNA expression in the hypoxic heart was only significantly different in day 14, whereas, Apelin mRNA expression had showed significantly higher values starting from day 7 onward. This is in line with the evidence of cardiac hypertrophy based on histopathologic examination present from day 7 onwards. BNP-45 and Apelin-13 levels were significantly higher compared to control from day 5 onwards with a peak on day 7. Although significantly higher than control, Apelin-13 and BNP-45 level decreases in day 14 as compared to day 7. Mean APJ levels showed a similar profile with Apelin-13 and BNP-45 levels with a peak in day 7 (4.619 ng/mL). The cardiac Apelin-13 level shows strong significant correlation with BNP-45 levels (r 0.823, p-value 0.0001). There was also a strong significant correlation between APJ receptor levels with Apelin-13 (r 0.9029, p-value 0.001) and BNP-45 (r 0.9062, p-value 0.0009) levels. Apelin-13, APJ and BNP-45 levels also showed strong significant positive correlation to the duration of hypoxia exposure. Conclusion Chronic (≥5 days) and not acute systemic hypoxia in an experimental rat model leads to increase in Apelin-13, APJ and BNP-45 levels. Apelin-13 and BNP-45 were found to significantly increase from 5 days onwards. Apelin mRNA expression was found to show significant increase earlier compared to BNP-45 mRNA expression. Hence, Apelin may serve as a new candidate biomarker for detection of HF due to oxidative stress compared to BNP-45. Exposure to chronic systemic hypoxia can serve as an easily replicable rat model for heart failure. Acknowledgement/Funding Department of Biochemistry and Molecular Biology, Faculty of Medicine, Tarumanagara University, Jakarta, Indonesia

Effects of triiodo-thyronine on angiotensin-induced cardiomyocyte hypertrophy: reversal of increased β-myosin heavy chain gene expression

2006 ◽  
Vol 84 (8-9) ◽  
pp. 935-941 ◽  
Author(s):  
Baohua Wang ◽  
Jingping Ouyang ◽  
Zhengyuan Xia
Keyword(s):  
Gene Expression ◽  
Angiotensin Ii ◽  
Thyroid Hormone ◽  
Cardiac Hypertrophy ◽  
Atpase Activity ◽  
Mrna Expression ◽  
Myosin Heavy Chain ◽  
Heavy Chain ◽  
Ang Ii ◽  
Hypertrophic Growth

Thyroid hormone-induced cardiac hypertrophy is similar to that observed in physiological hypertrophy, which is associated with high cardiac contractility and increased α-myosin heavy chain (α-MHC, the high ATPase activity isoform) expression. In contrast, angiotensin II (Ang II) induces an increase in myocardial mass with a compromised contractility accompanied by a shift from α-MHC to the fetal isoform β-MHC (the low ATPase activity isoform), which is considered as a pathological hypertrophy and inevitably leads to the development of heart failure. The present study is designed to assess the effect of thyroid hormone on angiotensin II-induced hypertrophic growth of cardiomyocytes in vitro. Cardiomyocytes were prepared from hearts of neonatal Wistar rats. The effects of Ang II and 3,3′,5-triiodo-thyronine (T3) on incorporations of [3H]-thymine and [3H]-leucine, MHC isoform mRNA expression, PKC activity, and PKC isoform protein expression were studied. Ang II enhanced [3H]-leucine incorporation, β-MHC mRNA expression, PKC activity, and PKCε expression and inhibited α-MHC mRNA expression in cardiomyocytes. T3 treatment prevented Ang II-induced increases in PKC activity, PKCε, and β-MHC mRNA overexpression and favored α-MHC mRNA expression. Thyroid hormone appears to be able to reprogram gene expression in Ang II-induced cardiac hypertrophy, and a PKC signal pathway may be involved in such remodeling process.

Increased endothelin-1 and endothelin receptor expression in myocytes of ischemic and reperfused rat hearts and ventricular myocytes exposed to ischemic conditions and its inhibition by nitric oxide generation

2003 ◽  
Vol 81 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Xiaohong Tracey Gan ◽  
Subrata Chakrabarti ◽  
Morris Karmazyn
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Ventricular Myocytes ◽  
Receptor Expression ◽  
Neonatal Rat ◽  
No Donor ◽  
Myocardial Ischemia And Reperfusion ◽  
Endothelin 1 ◽  
Hypoxic Conditions ◽  
Rat Hearts

Endothelin-1 (ET-1) and nitric oxide (NO) exert opposite effects in the cardiovascular system, and there is evidence that the NO counters the potential deleterious effects of ET-1. We investigated whether NO affects the increased mRNA expression of ET-1 and endothelin receptors induced by (i) 30 min of ischemia with or without 30 min reperfusion in myocytes from isolated rat hearts or (ii) ischemic conditions (acidosis or hypoxia) in cultured rat neonatal ventricular myocytes. Ischemia with or without reperfusion produced more than a twofold increase in mRNA expression of ET-1 as well as the ETAand ETBreceptor (P < 0.05), although these effects were completely blocked by the NO donor 3-morpholinosydnonimine (SIN-1; 1 μM). To assess the possible factors regulating ET expression, myocytes were exposed to acidosis (pH 6.8–6.2) or to hypoxic conditions in an anaerobic chamber for 24 h in the presence or absence of SIN-1. At all acidic pHs, ET-1 and ETAreceptor mRNA expression was significantly (P < 0.05) elevated approximately threefold, although the magnitude of elevation was independent of the degree of acidosis. These effects were completely prevented by SIN-1. ETBreceptor expression was unaffected by acidosis. Hypoxia increased ET-1 as well as ETAand ETBreceptor expression threefold (P < 0.05), although this was unaffected by SIN-1. Our results demonstrate that myocardial ischemia and reperfusion upregulate the ET system, which is inhibited by NO. Although increased expression of the ET system can be mimicked by both acidosis and hypoxia, only the effects of the former are NO sensitive. NO may serve an endogenous inhibitory factor which regulates the expression of the ET system under pathological conditions.Key words: ET-1, ET receptors, NO, neonatal rat ventricular myocytes, hypoxia, acidosis.

scholarly journals Over, and Underexpression of Endothelin 1 and TGF-Beta Family Ligands and Receptors in Lung Tissue of Broilers with Pulmonary Hypertension

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Norma Dominguez-Avila ◽  
Gabriel Ruiz-Castañeda ◽  
Javier González-Ramírez ◽  
Nora Fernandez-Jaramillo ◽  
Jorge Escoto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pulmonary Hypertension ◽  
Mrna Expression ◽  
Cardiac Failure ◽  
Transforming Growth Factor Beta ◽  
Transforming Growth Factor ◽  
Control Group ◽  
Endothelin 1 ◽  
Mrna Gene ◽  
Mrna Gene Expression

Transforming growth factor beta (TGFβ) is a family of genes that play a key role in mediating tissue remodeling in various forms of acute and chronic lung disease. In order to assess their role on pulmonary hypertension in broilers, we determined mRNA expression of genes of the TGFβfamily and endothelin 1 in lung samples from 4-week-old chickens raised either under normal or cold temperature conditions. Both in control and cold-treated groups of broilers, endothelin 1 mRNA expression levels in lungs from ascitic chickens were higher than levels from healthy birds (), whereas levels in animals with cardiac failure were intermediate. Conversely, TGFβ2 and TGFβ3 gene expression in lungs were higher in healthy animals than in ascitic animals in both groups (). TGFβ1, TβRI, and TβRII mRNA gene expression among healthy, ascitic, and chickens with cardiac failure showed no differences (). BAMBI mRNA gene expression was lowest in birds with ascites only in the control group as compared with the values from healthy birds ().

Epigenetic control of exercise training-induced cardiac hypertrophy by miR-208

2016 ◽  
Vol 130 (22) ◽  
pp. 2005-2015 ◽  
Author(s):  
Ursula Paula Renó Soci ◽  
Tiago Fernandes ◽  
Valerio Garrone Barauna ◽  
Nara Yumi Hashimoto ◽  
Gloria de Fátima Alves Mota ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Target Genes ◽  
Aerobic Training ◽  
Therapeutic Potential ◽  
Down Regulation ◽  
Epigenetic Control ◽  
Cardiac Gene Expression ◽  
Cardiac Gene

The physiological training-induced cardiac hypertrophy is epigenetically orchestrated by up-regulation of miR-208a/miR-208b and down-regulation of their target genes: Sox6, Med13, Purβ, SP3 and HP1β. These results highlight the therapeutic potential of aerobic training and miR-208 in cardiac gene expression.

Effects of exercise training on pathological cardiac hypertrophy related gene expression and apoptosis

2006 ◽  
Vol 97 (2) ◽  
pp. 216-224 ◽  
Author(s):  
Young I. Lee ◽  
Joon Y. Cho ◽  
Mun H. Kim ◽  
Kee B. Kim ◽  
Dong J. Lee ◽  
...  
Keyword(s):  
Gene Expression ◽  
Exercise Training ◽  
Cardiac Hypertrophy ◽  
Related Gene ◽  
Pathological Cardiac Hypertrophy
Sign in / Sign up

Export Citation Format

Share Document