[Home ] [Archive]   [ فارسی ]  
:: Main :: About :: Current Issue :: Archive :: Search :: Submit :: Contact ::
Main Menu
Home::
Journal Information::
Indexing Sources::
Guide for Authors::
Online Submission::
Ethics::
Articles archive::
For Reviewers::
Contact us::
::
Basic and Clinical Biochemistry and Nutrition
..
DOAJ
..
CINAHL
..
EBSCO
..
IMEMR
..
ISC
..
Search in website

Advanced Search
..
Receive site information
Enter your Email in the following box to receive the site news and information.
..
enamad
..
:: Volume 24, Issue 4 (Bimonthly 2020) ::
Feyz 2020, 24(4): 357-365 Back to browse issues page
Effect of moderate intensity exercise on HDAC4 and CaMKII genes expression in myocardium of male rats
Mojdeh Khajehlandi , Lotfali Bolboli , Marefat Siahkuhian , Mohammad Rami , Mohammadreza Tabandeh
Department of Physical Education and Sport Sciences, Faculty of Educational Sciences and Psychology, University of Mohaghegh Ardabili, Ardabil, I.R. Iran. , l_bolboli@uma.ac.ir
Abstract:   (2177 Views)
Background: Histone Dacetylases-4 (HDAC4) is phosphorylated by calcium-calmodulin-dependent kinase (CaMKII) that plays an important role in cardiac tissue hypertrophy. Therefore, the present study aimed to investigate the effect of moderate intensity exercise on HDAC4 and CaMKII genes expression in myocardial Wistar male rats.
Materials and Methods: In this experimental study, 19 adult male rats with 10 weeks of age and weighing of (243±8.2 g) were divided into 2 groups (endurance training=9) and (control=10) based on weight matching. Training program consisted of 6 weeks of endurance training, 5 days per week and moderate intensity. 24 hours after the last training session, cardiac tissue samples were extracted to measure the expression levels of HDAC4 and CaMKII by in vitro Real Time PCR. Data were analyzed using SPSS software version 23 and independent t-test was used.
Results: The results showed that the expression of both HDAC4 and CaMKII genes in the exercise group was lower than the control group, significantly (P<0.001).
Conclusion: According to the results of the present study, it seems that moderate intensity endurance training can change some factors related to cardiac hypertrophy tissue of rats and can be effective in preventing cardiovascular disease.
Keywords: Moderate intensity endurance training, HDAC4, CaMKII, Myocard, Male rats
Full-Text [PDF 1445 kb]   (753 Downloads)    
Type of Study: Research | Subject: General
Received: 2020/02/17 | Revised: 2020/10/10 | Accepted: 2020/08/5 | Published: 2020/10/10
References
1. Seo DY, Kwak HB, Kim AH, Park SH, Heo JW, Kim HK, et al. Cardiac adaptation to exercise training in health and disease. Pflug Arch Eur J PHY 2020; 472(2): 155-68.
2. Basavarajaiah S, Boraita A, Whyte G, Wilson M, Carby L, Shah A, et al. Ethnic differences in left ventricular remodeling in highly trained athletes relevance to differentiating physiologic left ventricular hypertrophy from hypertrophic cardiomyopathy. J Am Coll Cardiol 2008; 51(23): 2256-62.
3. Henriksen E, Sundstedt M, Hedberg P. Left ventricular end-diastolic geometrical adjustments during exercise in endurance athletes. Clin Physiol Funct Imaging 2008; 28(2): 76-80.
4. Anderson E, Durstine JL. Physical activity, exercise, and chronic diseases: A brief review. Sports Medicine Health Science 2019; 1(1): 3-10.
5. Ntanasis-Stathopoulos J, Tzanninis JG, Philippou A, Koutsilieris M. Epigenetic regulation on gene expression induced by physical exercise. J Musculoskelet Neuronal Interact 2013; 13(2): 133-46.
6. Liu Y, Randall WR, Schneider MF. Activity-dependent and independent nuclear fluxes of HDAC6 mediated by different kinases in adult skeletal muscle. J Cell Biol 2005; 146:661-71.
7. McKinsey TA, Zhang CL, Olson EN. Signaling chromatin to make muscle. CURR OPIN CELL BIOL 2002; 14(6): 763-72.
8. Jaenisch, Wolffe, Bird, Fedoroff, Horz, Finnegan, Laird, Flavell, Wilkins, Allshire, Kooter. DNA methylation, nucleosomes and the inheritance of chromatin structure and function-Discussion. 1995: 35-45.
9. Miska EA, Karlsson C, Langley E, Nielsen SJ, Pines J, Kouzarides T. HDAC4 deacetylase associates with and represses the MEF2 transcription factor. EMBO J 1999; 18(18): 5099-107.
10. Kehat I, Accornero F, Aronow BJ, Molkentin JD. Modulation of chromatin position and gene expression by HDAC4 interaction with nucleoporins. J Cell Biol 2011; 193(1): 21-9.
11. Dressel U, Bailey PJ, Wang SM, Downes M, Evans RM, Muscat GE. A dynamic role for HDAC7 in MEF2-mediated muscle differentiation. J BIOL CHEM 2001; 276(20):17007-13.
12. Rose AJ, Frosig C, Kiens B, Wojtaszewski JFP, Richter EA. Effect of endurance exercise training on Ca2+calmodulin-dependent protein kinase II expression and signalling in skeletal muscle of humans. J Physiol 2007; 583(2): 785-95.
13. Feng J, Fouse S, Fan G. Epigenetic regulation of neural gene expression and neuronal function. Pediatr Res 2007; 61(5):58-63.
14. Wang AH, Bertos NR, Vezmar M, Pelletier N, Crosato M, Heng HH, et al. HDAC4, a human histone deacetylase related to yeast HDA1, is a transcriptional corepressor. Mol Cell Biol 1999; 19 (11):7816-27.
15. Backs J, Song K, Bezprozvannaya S, Chang S, Olson EN. CaM kinase II selectively signals to histone deacetylase 4 during cardiomyocyte hypertrophy. J Clin Invest 2006; 116 (7):1853-64.
16. Zhang T, Maier LS, Dalton ND, Miyamoto S, Ross J, Bers DM, et al. The δ C isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure. Circulation Res 2003; 92: 912-9.
17. Zhang T, Miyamoto S, Brown JH. Cardiomyocyte calcium and calcium/calmodulin-dependent protein kinase II: friends or foes?. Recent Prog Horm Res 2004; 59: 141-68.
18. Zhang T, Brown JH. Role of Ca2+/calmodulin dependent protein kinase II in cardiac hypertrophy and heart failure. Cardiovascular Res 2004; 63: 476-86.
19. Potthoff MJ, Wu H, Arnold MA, Shelton JM, Backs J, McAnally J, et al. Histone deacetylase degradation and MEF2 activation promote the formation of slow-twitch myofibers. J Clin Invest 2007; 117(9): 2459-67.
20. Rose AJ, Frosig C, Kiens B, Wojtaszewski JFP, Richter EA. Effect of endurance exercise training on Ca2+calmodulin-dependent protein kinase II expression and signalling in skeletal muscle of humans. J Physiol 2007; 583(2): 785-95.
21. Piraki P, Hematfar A, Behpour N, Samavati Sharifi MA. The Effect of 10 Weeks of Exhaustive Swimming on Gene Expression of Histone Deacetylase-4 and Myocyte Enhancer Factor-2c in Left Ventricle in Male Rats. Journal of sport Biosciences 2018; 10(2): 249-61. [in Persian]
22. Fathi M, Gharakanlou R, Rezaei R. The Effect of 14-Week Endurance Training on Left Ventricle HDAC4 Gene Expression of Wistar Male Rat. J Sport Biomotor Sci 2013; 11(1): 5-15.
23. 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.
24. Rose AJ, Kiens B, Richter EA. Ca2+– calmodulin‐dependent protein kinase expression and signalling in skeletal muscle during exercise. J Physiol 2006; 574(3): 889-903.
25. Kemi OJ, Ellingsen Ø, Ceci M, Grimaldi S, Smith GL, Condorelli G, et al. Aerobic interval training enhances cardiomyocyte contractility and Ca 2+ cycling by phosphorylation of CaMKII and Thr-17 of phospholamban. J Mol Cell Cardiol 2007; 43(3): 354-61
26. Chae CH, Jung SL, An SH, Jung CK, Nam SN, Kim HT. Treadmill exercise suppresses muscle cell apoptosis by increasing nerve growth factor levels and stimulating p-phosphatidylinositol 3-kinase activation in the soleus of diabetic rats & quot. Physiol Biochem 2011; 67(2): 235-41.
27. Alessio DL, Laura S, Gianni P, Stefano P, Giorgio G. The effect of exercise training on left ventricular function in young elite athletes. Cardiovasc Ultrasound 2011; 9: 27.
28. Da Silva JND, Fernandes T, Soci UPR, Monteiro AWA, Phillips MI, De Oliveira EM. Swimming training in rats increases cardiac MicroRNA-126 expression and angiogenesis. Med Sci Sports Exerc 2012; 44(8): 1453-62.
29. DeBosch B, Treskov I, Lupu TS, Weinheimer C, Kovacs A, Courtois M, et al. Akt1 is required for physiological cardiac growth. Circulation 2006; 113(17):2097-104.
30. O'Neill BT, Kim J, Wende AR, Theobald HA, Tuinei J, Buchanan J, et al. A conserved role for phosphatidylinositol 3-kinase but not Akt signaling in mitochondrial adaptations that accompany physiological cardiac hypertrophy. Cell Metab 2007; 6 (4):294-306.
31. Liu F, Pore N, Kim M, Voong KR, Dowling M, Maity A, et al. Regulation of histone deacetylase 4 expression by the SP family of transcription factors. Mol Biol Cell 2006; 17(2): 585-97.
32. Bolboli L, Khajehlandi M. A Comparison of the Effect of Endurance Training on the Activities of Glutathione Peroxidase and Superoxide Dismutase in the Cardiac Tissue of Healthy and Diabetic Rats. Yafte 2020; 21(4): 20-31. [in Persian]
33. Zaha VG, Young LH. AMP-activated protein kinase regulation and biological actions in the heart. Circ Res 2012; 111(6): 800-14.
34. Musi N, Hirshman MF, Arad M, Xing Y, Fujii N, Pomerleau J, et al. Functional role of AMP-activated protein kinase in the heart during exercise. FEBS Lett 2005; 579(10): 2045-50.
35. Mihaylova MM, Vasquez DS, Ravnskjaer K, Denechaud PD, Yu RT, Alvarez JG, et al. Class IIa histone deacetylases are hormone-activated regulators of FOXO and mammalian glucose homeostasis. Cell 2011; 145 (4):607-21.
36. Zhang T, Brown JH. Role of Ca2+/calmodulin dependent protein kinase II in cardiac hypertrophy and heart failure. Cardiovascular Res 2004; 63: 476-86.
37. Anderson ME, Braun AP, Wu Y, Lu T, Wu Y, Schulman H, et al. KN-93, an inhibitor of multifunctional Ca++/calmodulin-dependent protein kinase, decreases early afterdepolarizations in rabbit heart. J Pharmacol Exp Ther 1998; 287(3):996–1006.
38. Wu Y, Roden DM, Anderson ME. Calmodulin kinase inhibition prevents development of the arrhythmogenic transient inward current. Circ Res 1999; 84(8): 906–12.
39. Wu Y, MacMillan LB, McNeill RB, Colbran RJ, Anderson ME. CaM kinase augments cardiac Ltype Ca2+ current: a cellular mechanism for long Q-T arrhythmias. Am J Physiol 1999; 276(6 Pt 2): H2168-2178.
40. Kirchhefer U, Schmitz W, Scholz H, Neumann J. Activity of cAMP-dependent protein kinase and Ca2+/calmodulin-dependent protein kinase in failing and nonfailing human hearts. Cardiovasc Res 1999; 42(1): 254–61
41. Kehat I, Accornero F, Aronow BJ, Molkentin JD. Modulation of chromatin position and gene expression by HDAC4 interaction with nucleoporins. J Cell Biol 2011; 193(1):21-9.
42. Powers SK, Quindry JC, Kavazis AN. Exercise-induced cardioprotection against myocardial ischemiareperfusion injury. Free Radic Biol Med 2008; 44: 193-201.
43. Naderi R, Gisou M, Mohammadi M, Ghaznavi R, Ghyasi R, Vatankhah A. Voluntary Exercise Protects Heart from Oxidative Stress in Diabetic Rats. Adv Pharm Bull 2015; 5(2): 231-6.
44. Anderson ME, Brown JH, Bers DM. CaMKII in myocardial hypertrophy and heart failure. J Mol Cell Cardiol 2011; 51(4): 468–73.
Send email to the article author

Add your comments about this article
Your username or Email:

CAPTCHA


XML   Persian Abstract   Print


Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:

Khajehlandi M, Bolboli L, Siahkuhian M, Rami M, Tabandeh M. Effect of moderate intensity exercise on HDAC4 and CaMKII genes expression in myocardium of male rats. Feyz 2020; 24 (4) :357-365
URL: http://feyz.kaums.ac.ir/article-1-4089-en.html


Creative Commons License
This open access journal is licensed under a Creative Commons Attribution-NonCommercial ۴.۰ International License. CC BY-NC ۴. Design and publishing by Kashan University of Medical Sciences.
Copyright ۲۰۲۳© Feyz Medical Sciences Journal. All rights reserved.
Volume 24, Issue 4 (Bimonthly 2020) Back to browse issues page
مجله علوم پزشکی فیض Feyz Medical Sciences Journal
Persian site map - English site map - Created in 0.05 seconds with 46 queries by YEKTAWEB 4645