scholarly journals Reduction in Left Ventricular Messenger RNA for Transforming Growth Factor β 1 Attenuates Left Ventricular Fibrosis and Improves Survival Without Lowering Blood Pressure in the Hypertensive TGR(mRen2)27 Rat

Hypertension ◽  
2000 ◽  
Vol 36 (5) ◽  
pp. 747-754 ◽  
Author(s):  
Yigal M. Pinto ◽  
Sara-Joan Pinto-Sietsma ◽  
Tobias Philipp ◽  
Sonja Engler ◽  
Peter Koβmehl ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Factor ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Left Ventricular ◽  
Ventricular Fibrosis

Enalapril decreases cardiac mass and fetal gene expression without affecting the expression of endothelin-1, transforming growth factor β-1, or cardiotrophin-1 in the healthy normotensive rat

2011 ◽  
Vol 89 (3) ◽  
pp. 197-205 ◽  
Author(s):  
Katarina Mackovicova ◽  
Andrea Gazova ◽  
Dana Kucerova ◽  
Beata Gajdacova ◽  
Jan Klimas ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Growth Factors ◽  
Angiotensin Ii ◽  
Growth Factor ◽  
Cardiac Hypertrophy ◽  
Left Ventricular Mass ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Left Ventricular ◽  
Ventricular Mass

Angiotensin II can induce cardiac hypertrophy by stimulating the release of growth factors. ACE inhibitors reduce angiotensin II levels and cardiac hypertrophy, but their effects on the healthy heart are largely unexplored. We hypothesized that ACE inhibition decreases left ventricular mass in normotensive animals and that this is associated with altered expression of cardiac fetal genes, growth factors, and endothelial nitric oxide synthase (eNOS). Wistar rats (n = 7 per group) were orally administered with enalapril twice daily for a total daily dose of 5 mg·kg–1·d–1 (ENAP5) or 15 mg·kg–1·d–1 (ENAP15) or vehicle. Systolic blood pressure was measured by the tail-cuff method. Left ventricular expression of cardiac myosin heavy chain-α (MYH6) and -β (MYH7), atrial natriuretic peptide (ANP), endothelin-1 (ET-1), transforming growth factor β-1 (TGFβ-1), cardiotrophin-1 (CT-1), and renal renin were examined by real-time PCR, and eNOS using Western blot. Blood pressure was decreased only in ENAP15 animals (p < 0.05 vs. Control), whereas left ventricular mass decreased after both doses of enalapril (p < 0.05 vs. Control). MYH7 and ANP were reduced in ENAP15, while no changes in ET-1, TGFβ-1, CT-1, and MYH6 mRNA or eNOS protein were observed. Renal renin dose-dependently increased after enalapril treatment. Enalapril significantly decreased left ventricular mass even after 1 week treatment in the normotensive rat. This was associated with a decreased expression of the fetal genes MYH7 and ANP, but not expression of ET-1, CT-1, or TGFβ-1.

Abstract 297: Cardiac Transforming-growth-factor β-stimulated Clone 22 Gene Expression By Hypertrophic Stimuli

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Annina Kelloniemi ◽  
Jani Aro ◽  
Elina Koivisto ◽  
Heikki Ruskoaho ◽  
Jaana Rysä
Keyword(s):  
Growth Factor ◽  
Gene Transfer ◽  
Transforming Growth Factor ◽  
Pressure Overload ◽  
Transforming Growth Factor Β ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Mrna Levels ◽  
Ang Ii ◽  
Sd Rats

Objectives: Transforming-growth-factor β-stimulated clone 22 (TSC-22) is a leucine zipper protein expressed in many tissues and possessing various transcription-modulating activities. However, its function in the heart remains largely unknown. The aim of the present study was to characterize the cardiac TSC-22 expression. Methods: Acute pressure overload was accomplished in conscious Sprague-Dawley (SD) rats by intravenous infusion of arginine 8 -vasopressin (AVP, 0.05 μg/kg/min) for 4 hours and subcutaneous infusion of angiotensin II (Ang II, 33 μg/kg/h) with and without Ang II receptor type 1 blocker losartan (400 μg/kg/h) by using osmotic minipumps for 2 weeks. Adenovirus-mediated intramyocardial gene transfer of TSC-22 was performed into left ventricle (LV) of SD rats. Experimental myocardial infarction (MI) was produced by ligation of the left anterior descending coronary artery. Cultured neonatal rat ventricular myocytes (NRVM) were treated with endothelin-1 (ET-1, 100 nM). Results: A significant 1.6-fold increase ( P <0.05) in LV TSC-22 mRNA levels was noted already after 1 hour AVP infusion. Moreover, Ang II infusion markedly upregulated TSC-22 expression, LV mRNA levels being highest at 6 hours (11-fold, P <0.001). Simultaneous infusion of losartan completely abolished Ang II-induced increase in TSC-22 mRNA levels. Adenovirus-mediated gene transfer of TSC-22 into LV resulted a 1.9-fold ( P <0.001) increase in TSC-22 mRNA levels, accompanied by upregulated BNP mRNA levels (1.4-fold, P <0.01). In response to experimental MI, TSC-22 mRNA levels were elevated 4.1-fold ( P <0.001) at 1 day and 1.9-fold ( P <0.05) at 4 weeks. In cultured NRVM, ET-1 treatment increased TSC-22 mRNA levels from 1 h to 24 h, the greatest increase being observed at 12 h (2.7-fold, P <0.001). TSC-22 protein levels were upregulated from 4 h to 24 h with the highest increase at 24 h (4.7-fold, P <0.01). Conclusion: These results indicate that TSC-22 expression is rapidly activated in response to pressure overload, MI and in ET-1 treated cultured NRVM. Moreover, adenovirus-mediated overexpression of TSC-22 mRNA was associated with elevated left ventricular BNP mRNA levels.

scholarly journals Cardiomyopathy in young adults with classic mitral valve prolapse

2013 ◽  
Vol 24 (4) ◽  
pp. 694-701 ◽  
Author(s):  
Eduard Malev ◽  
Svetlana Reeva ◽  
Lyubov Vasina ◽  
Eugeny Timofeev ◽  
Asiyet Pshepiy ◽  
...  
Keyword(s):  
Young Adults ◽  
Growth Factor ◽  
Mitral Valve ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Mitral Valve Prolapse ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Left Ventricular ◽  
Control Group

AbstractBackground: In some inherited connective tissue diseases with involvement of the cardiovascular system, for example, Marfan syndrome, early impairment of left ventricular function, which have been described as Marfan-related cardiomyopathy has been reported. Our aim was to evaluate the left ventricular function in young adults with mitral valve prolapse without significant mitral regurgitation using two-dimensional strain imaging and to determine the possible role of the transforming growth factor-β pathway in its deterioration. Methods: We studied 78 young adults with mitral valve prolapse without mitral regurgitation in comparison with 80 sex-matched and age-matched healthy individuals. Longitudinal strain and strain rates were defined using spackle tracking. Concentrations of transforming growth factor-β1 and β2 in serum were determined by enzyme-linked immunosorbent assays. Results: In 29 patients, classic relapse was identified with a leaflet thickness of ≥ 5 mm; 49 patients had a non-classic mitral valve prolapse. Despite the similar global systolic function, a significant reduction in global strain was found in the classic group (−15.5 ± 2.9%) compared with the non-classic group (−18.7 ± 3.8; p = 0.0002) and the control group (−19.6 ± 3.4%; p < 0.0001). In young adults with non-classic prolapse, a reduction in longitudinal deformation was detected only in septal segments. Transforming growth factor-β1 and β2 serum levels were elevated in patients with classic prolapse as compared with the control group and the non-classic mitral valve prolapse group. Conclusions: These changes in the deformations may be the first signs of deterioration of the left ventricular function and the existence of primary cardiomyopathy in young adults with mitral valve prolapse, which may be caused by increased transforming growth factor-β signalling.

scholarly journals Transforming Growth Factor-β Protein and Messenger RNA Expression Is Increased in the Closing Ductus Arteriosus

1996 ◽  
Vol 39 (3) ◽  
pp. 427-434 ◽  
Author(s):  
Jaime E Tannenbaum ◽  
Nahid S Waleh ◽  
Françoise Mauray ◽  
Leslie Gold ◽  
Elizabeth A Perkett ◽  
...  
Keyword(s):  
Growth Factor ◽  
Messenger Rna ◽  
Transforming Growth Factor ◽  
Ductus Arteriosus ◽  
Transforming Growth Factor Β ◽  
Rna Expression ◽  
Β Protein

scholarly journals Transforming growth factor β receptor inhibition prevents ventricular fibrosis in a mouse model of progressive cardiac conduction disease

2017 ◽  
Vol 113 (5) ◽  
pp. 464-474 ◽  
Author(s):  
Mickael Derangeon ◽  
Jérôme Montnach ◽  
Cynthia Ore Cerpa ◽  
Benoit Jagu ◽  
Justine Patin ◽  
...  
Keyword(s):  
Growth Factor ◽  
Mouse Model ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Cardiac Conduction ◽  
Receptor Inhibition ◽  
Β Receptor ◽  
Ventricular Fibrosis

scholarly journals Effect of Lifestyle Modification and Metformin on Fetuin-A and Transforming Growth Factor-ß (TGF- ß) in Metabolic Syndrome

2019 ◽  
Vol 1 (1) ◽  
Author(s):  
Melati Silvanni Nasution ◽  
Dharma Lindarto
Keyword(s):  
Blood Pressure ◽  
Metabolic Syndrome ◽  
Placebo Group ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Lifestyle Modification ◽  
Density Lipoprotein ◽  
Transforming Growth Factor Β ◽  
Fetuin A ◽  
Metformin Group

Fetuin-A is a liver-synthesized protein that is secreted into serum. Transforming growth factor-β (TGF-β) is a polypeptide member of the TGF-β superfamily of cytokines. The purpose of this study is to evaluate the effects of lifestyle modification and metformin on fetuin-A and Transforming Growth Factor-ß (TGF- ß) in metabolic syndrome (MetS). Forty MetS subjects were randomly assigned to treatment with placebo (n=20) or metformin (n=20) in addition to lifestyle modification for 12 weeks. All 40 participants completed the study. After 12 weeks, both groups had significant reductions in weight, body mass index (BMI), waist circumference (WC), systolic blood pressure (SBP) and diastolic blood pressure (DBP) (all p<0.001). The placebo group also had significant improvement in fasting plasma glucose (FPG) and C-reactive protein (CRP) (p<0,001 ; p<0.05 respectively). Weight, BMI, WC, FPG, 2-hour postprandial glucose (2h-PPG), high density lipoprotein cholesterol (HDL-C), triglycerides (TG), fetuin-A and TGF- ß in the metformin group decreased significantly compared to the placebo group. Reduction of plasma fetuin-A was significantly associated with TG in the metformin group. Lifestyle modification and treatment with metformin for 12 weeks improved cardio-metabolic risk factors in MetS and reduced fetuin-A levels.

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