Document Type : Research Paper
Authors
Abstract
Endurance activity causes changes in the expression of some genes and induces hypertrophy in heart, Meanwhile Hand2 gene is changed in response to pathological hypertrophy of the heart, so the aim of this study was to investigate the effect of endurance activity on Hand2 gene expression in left ventricle. For this purpose, 14 rats (male wistar, 113±20g, age five weeks) under controlled conditions (temperature, light/dark (12:12) cycle, with ad Libitum access to food and water) were housed and randomly divided into control and Experimental groups, the experimental group performed 14 -weeks endurance training on motorized treadmill, and then were anesthetized and sacrificed 48 hours after the end of the last session. The left ventricle of the heart was removed. Real time RT-PCR method was used to determine the expression levels of Hand2 in the left ventricle. the obtained data were evaluated using t-test. The results showed, the mean of left ventricle Hand2 gene expression increased in experimental group significantly (P=0.007) than control group. It seems, Hand2 gene influence on created the type of hypertrophy.
Keywords
1) Wisloff U, Helgerud J, Kemi OJ, Ellingsen O. Intensity-controlled treadmill running in rats: VO (2 max) and cardiac hypertrophy. Am J Physiol Heart Circ Physiol. 2001; 280 (3): 1301-10.
2) Medeiros A, Oliveira EM, Gianolla R, Casarini DE, Negrao CE, Brum PC. Swimming training increases cardiac vagal activity and induces cardiac hypertrophy in rats. Braz J Med Biol Res. 2004; 37 (12):1909-17.
3) Rohini A, Agrawal N, Koyani CN, Singh R. Molecular targets and regulators of cardiac hypertrophy. Pharmacological Research. 2010; 61 (4):269-80.
4) Luedde M, Katus HA, Frey N. Novel molecular targets in the treatment of cardiac hypertrophy. Recent Pat Cardiovasc Drug Discov. 2006; 1 (1):1-20.
5) McMullen. J R, Jennings. J L. Differences between pathological and physiological cardiac hypertrophy: novel therapeutic strategies to treat heart failure. Clinical and Experimental Pharmacology and Physiology. 2007; 34:255-62.
6) Srivastava D, Cserjesi P, Olson EN. A subclass of bHLH proteins required for cardiac morphogenesis. Science. 1995; 270 (5244):1995-9.
7) Dai YS, Cserjesi P. The basic helix-loop-helix factor, HAND2, functions as a transcriptional activator by binding to E-boxes as a heterodimer. J Biol Chem. 2002; 277 (15):12604-12.
8) Massari ME, Murre C. Helix-loop-helix proteins: regulators of transcription in eucaryotic organisms. Mol Cell Biol. 2000; 20 (2):429-40.
9) Firulli BA, Hadzic DB, McDaid JR, Firulli AB. The basic helix-loop-helix transcription factors dHAND and eHAND exhibit dimerization characteristics that suggest complex regulation of function. J Biol Chem. 2000; 275 (43):33567-73.
10) Togi K, Yoshida Y, Matsumae H, Nakashima Y, Kita T, Tanaka M. Essential role of Hand2 in interventricular septum formation and trabeculation during cardiac development. Biochem Biophys Res Commun. 2006; 343 (1):144-51.
11) Akazawa H, Komuro I. Roles of cardiac transcription factors in cardiac hypertrophy. Circ Res. 2003; 92 (10):1079-88.
12) Srivastava D. HAND proteins: molecular mediators of cardiac development and congenital heart disease. Trends Cardiovasc Med. 1999; 9 (1-2):11-8.
13) Zhao Y, Srivastava D, Samal E. Serum response factor regulates a muscle-specific microRNA that targets Hand2 during cardiogenesis. Nature. 2005; 436 (7048):214-20.
14) McFadden DG, Barbosa AC, Richardson JA, Schneider MD, Srivastava D, Olson EN. The Hand1 and Hand2 transcription factors regulate expansion of the embryonic cardiac ventricles in a gene dosage-dependent manner. Development. 2005; 132 (1): 189-201.
15) Thattaliyath BD, Livi CB, Steinhelper ME, Toney GM, Firulli AB. HAND1 and HAND2 are expressed in the adult-rodent heart and are modulated during cardiac hypertrophy. Biochem Biophys Res Commun. 2002; 297 (4):870-5.
16) Natarajan A, Yamagishi H, Ahmad F, Li D, Roberts R, Matsuoka R, et al. Human eHAND, but not dHAND, is down-regulated in cardiomyopathies. J Mol Cell Cardiol. 2001; 33 (9):1607-14.
17) Jin H, Yang R, Li W, Lu H, Ryan AM, Ogasawara AK, et al. Effects of exercise training on cardiac function, gene expression, and apoptosis in rats. Am J Physiol Heart Circ Physiol. 2000; 279 (6):H2994-3002.
18) Sun L, Shen W, Liu Z, Guan S, Liu J, Ding S. Endurance exercise causes mitochondrial and oxidative stress in rat liver: effects of a combination of mitochondrial targeting nutrients. Life Sci. 2010; 86 (1-2):39-44.
19) Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and the 2-ΔΔct Method. Methods. 2001; 25 (4):402-8.
20) Yuan JS, Reed A, Chen F, Stewart CN, Jr. Statistical analysis of real-time PCR data. BMC Bioinformatics. 2006; 7:85-97.
21) Wong ML, Medrano JF. Real-time PCR for mRNA quantitation. Biotechniques. 2005; 39 (1):75-85.
22) Schmittgen TD, Livak KJ. Analyzing real-time PCR data by the comparative CT method. Nature Protocols. 2008; 3 (6):1101-8.
23) Pfaffl MW. A new mathematical model for relative quantification in real-time RT-PCR. Nucleic Acids Res. 2001; 29 (9):45.
24) Yamagishi H, Olson EN, Srivastava D. The basic helix-loop-helix transcription factor, dHAND, is required for vascular development. J Clin Invest. 2000; 105 (3): 261-70.
25) Fathi M, Gharakanlou R, Abroun S, Mokhtari-Dizaji M, Rezaei R. Considerations in the evaluation of cardiac changes following endurance training in male Wistar rats. yafteh. 2013; 15:112-23 (in Persian).
26) Morganroth J, Maron BJ, Henry WL, Epstein SE. Comparative left ventricular dimensions in trained athletes. Ann Intern Med. 1975; 82 (4):521-4.
27) Venckunas T, Lionikas A, Marcinkeviciene JE, Raugaliene R, Alekrinskis A, Stasiulis A. Echocardiographic parameters in athletes of different sports. Journal of sports science & medicine. 2008; 7 (1):151-6.
28) Mihl C, Dassen WR, Kuipers H. Cardiac remodelling: concentric versus eccentric hypertrophy in strength and endurance athletes. Neth Heart J. 2008; 16 (4):129-33.
29) Bankir L. Antidiuretic action of vasopressin: quantitative aspects and interaction between V1a and V2 receptor-mediated effects. Cardiovasc Res. 2001; 51 (3):372-90.
)