Share This Article:

Myosin Heavy Chain Expression and Oxidative Modifications in Diabetic Rat Hearts

Abstract Full-Text HTML Download Download as PDF (Size:490KB) PP. 248-256
DOI: 10.4236/ojapps.2012.24037    3,919 Downloads   5,610 Views   Citations

ABSTRACT

In this study, we tested the hypotheses that 1) diabetes-induced disturbances in cardiac my-ATPase activity would be attributed to not only myosin heavy chain (MHC) isoform transitions, but also reduced amounts in MHC protein; and 2) if diabetes results in declines in the MHC protein content, this change would relate to oxidative damage to MHC. Diabetes was induced by a single intraperitoneal injection of streptozotocin. After 6 weeks of injection, the left ventricles were excised for mechanical and biochemical analyses. Peak twitch tension and the rate of force development in papillary muscles were decreased by 23.4% and 34.1%, respectively. A 33.5% reduction in myofibrillar ATPase activity occurred in conjunction with a 9.5% decrease in MHC protein as well as MHC isoform transitions towards a slower phenotype. The decreased MHC content was not accompanied by elevations in carbonyl groups present in MHC. Whole muscle analyses indicated that the contents of malondialdehyde and reduced glutathione were elevated. These results suggest that decreases in the MHC content may be associated, at least in part, with a diabetes-related inactivation of cardiac my-ATPase and may not be due to accumulation of oxidative damage to protein.

Conflicts of Interest

The authors declare no conflicts of interest.

Cite this paper

M. Kuratani, K. Kanzaki, N. Yanaka, S. Matsunaga and M. Wada, "Myosin Heavy Chain Expression and Oxidative Modifications in Diabetic Rat Hearts," Open Journal of Applied Sciences, Vol. 2 No. 4, 2012, pp. 248-256. doi: 10.4236/ojapps.2012.24037.

References

[1] S. Wild, G. Roglic, A. Green, R. Sicree and H. King, “Global Prevalence of Diabetes: Estimates for the Year 2000 and Projections for 2030,” Diabetes Care, Vol. 27, No. 5, 2004, pp. 1047-1053. doi:10.2337/diacare.27.5.1047
[2] R. Tarquini, C. Lazzeri, L. Pala, C. M. Rotella and G. F. Gensini, “The Diabetic Cardiomyopathy,” Acta Diabetologica, Vol. 48, No. 3, 2011, pp. 173-181. doi:10.1007/s00592-010-0180-x
[3] R. Bottinelli, “Functional Heterogeneity of Mammalian Single Muscle Fibres: Do Myosin Isoforms Tell the Whole Story?” Pflügers Archiv, Vol. 443, No. 1, 2001, pp. 6-17. doi:10.1007/s004240100700
[4] E. M. McNally, R. Kraft, M. Bravo-Zehnder, D. A. Taylor and L. A. Leinwand, “Full-Length Rat Alpha and Beta Cardiac Myosin Heavy Chain Sequences. Comparisons Suggest a Molecular Basis for Functional Differences,” Journal of Molecular Biology, Vol. 210, No. 3, 1989, pp. 665-671. doi:10.1016/0022-2836(89)90141-1
[5] D. E. Harris, S. S. Work, R. K. Wright, N. R. Alpert and D. M. Warshaw, “Smooth, Cardiac and Skeletal Muscle Myosin Force and Motion Generation Assessed by CrossBridge Mechanical Interactions in vitro,” Journal of Muscle Research and Cell Motility, Vol. 15, No. 1, 1994, pp. 11-19. doi:10.1007/BF00123828
[6] L. E. Wold, A. F. Ceylan-Isik, C. X. Fang, X. Yang, S. Y. Li, N. Sreejayan, J. R. Privratsky and J. Ren, “Metallothionein Alleviates Cardiac Dysfunction in Streptozotocin-Induced Diabetes: Role of Ca2+ Cycling Proteins, NADPH Oxidase, Poly(ADP-Ribose) Polymerase and Myosin Heavy Chain Isozyme,” Free Radical Biology and Medicine, Vol. 40, No. 8, 2006, pp. 1419-1429. doi:10.1016/j.freeradbiomed.2005.12.009
[7] S. Boudina and E. D. Abel, “Diabetic Cardiomyopathy Revisited,” Circulation, Vol. 115, No. 25, 2007, pp. 32133223. doi:10.1161/CIRCULATIONAHA.106.679597
[8] N. D. Roe, D. P. Thomas and J. Ren, “Inhibition of NADPH Oxidase Alleviates Experimental Diabetes Induced Myocardial Contractile Dysfunction,” Diabetes, Obesity and Metabolism, Vol. 13, No. 5, 2011, pp. 465473. doi:10.1111/j.1463-1326.2011.01369.x
[9] E. Shen, Y. Li, Y. Li, L. Shan, H. Zhu, Q. Feng, J. M. Arnold and T. Peng, “Rac1 Is Required for Cardiomyocyte Apoptosis during Hyperglycemia,” Diabetes, Vol. 58, No. 10, 2009, pp. 2386-2395. doi:10.2337/db08-0617
[10] M. Aragno, R. Mastrocola, G. Alloatti, I. Vercellinatto, P. Bardini, S. Geuna, M. G. Catalano, O. Danni and G. Boccuzzi, “Oxidative Stress Triggers Cardiac Fibrosis in the Heart of Diabetic Rats,” Endocrinology, Vol. 149, No. 1, 2008, pp. 380-388. doi:10.1210/en.2007-0877
[11] G. D. Lamb and H. Westerblad, “Acute Effects of Reactive Oxygen and Nitrogen Species on the Contractile Function of Skeletal Muscle,” The Journal of Physiology, Vol. 589, No. 9, 2011, pp. 2119-2127. doi:10.1113/jphysiol.2010.199059
[12] R. M. Murphy, T. L. Dutka and G. D. Lamb, “Hydroxyl Radical and Glutathione Interactions Alter Calcium Sensitivity and Maximum Force of the Contractile Apparatus in Rat Skeletal Muscle Fibres,” The Journal of Physiology, Vol. 586, No. 8, 2008, pp. 2203-2216. doi:10.1113/jphysiol.2007.150516
[13] T. L. Dutka, J. P. Mollica and G. D. Lamb, “Differential Effects of Peroxynitrite on Contractile Protein Properties in Fastand Slow-Twitch Skeletal Muscle Fibers of Rat,” Journal of Applied Physiology, Vol. 110, No. 3, 2011, pp. 705-716. doi:10.1152/japplphysiol.00739.2010
[14] J. Mary, S. Vougier, C. R. Picot, M. Perichon, I. Petropoulos and B. Friguet, “Enzymatic Reactions Involved in the Repair of Oxidized Proteins,” Experimental Gerontology, Vol. 39, No. 8, 2004, pp. 1117-1123. doi:10.1016/j.exger.2004.06.008
[15] Y. Zhong, S. Ahmed, I. L. Grupp and M. A. Matlib, “Altered SR Protein Expression Associated with Contractile Dysfunction in Diabetic Rat Hearts,” American Journal of Physiology-Heart and Circulatory Physiology, Vol. 281, No. 3, 2001, pp. H1137-H1147.
[16] L. Cai, W. Li, G. Wang, L. Guo, Y. Jiang and Y. J. Kang, “Hyperglycemia-Induced Apoptosis in Mouse Myocardium: Mitochondrial Cytochrome C-Mediated Caspase-3 Activation Pathway,” Diabetes, Vol. 51, No. 6, 2002, pp. 1938-1948. doi:10.2337/diabetes.51.6.1938
[17] N. Takeda, P. Dominiak, D. Turck, H. Rupp and R. Jacob, “Myocardial Catecholamine Responsiveness of Spontaneously Hypertensive Rats as Influenced by Swimming Training,” Basic Research in Cardiology, Vol. 80, No. 4, 1985, pp. 384-391. doi:10.1007/BF01908182
[18] R. W. Tsika, R. E. Herrick and K. M. Baldwin, “Interaction of Compensatory Overload and Hindlimb Suspension on Myosin Isoform Expression,” Journal of Applied Physiology, Vol. 62, No. 6, 1987, pp. 2180-2186.
[19] M. M. Bradford, “A Rapid and Sensitive Method for the Quantitation of Microgram Quantities of Protein Utilizing the Principle of Protein-Dye Binding,” Analytical Biochemistry, Vol. 72, No. 1-2, 1976, pp. 248-254. doi:10.1016/0003-2697(76)90527-3
[20] K. Kanzaki, M. Kuratani, T. Mishima, S. Matsunaga, N. Yanaka, S. Usui and M. Wada, “The Effects of Eccentric Contraction on Myofibrillar Proteins in Rat Skeletal Muscle,” European Journal of Applied Physiology, Vol. 110, No. 5, 2010, pp. 943-952. doi:10.1007/s00421-010-1579-3
[21] M. Wada, N. Ham?l?inen and D. Pette, “Isomyosin Patterns of Single Type IIB, IID and IIA Fibres from Rabbit Skeletal Muscle,” Journal of Muscle Research and Cell Motility, Vol. 16, No. 3, 1995, pp. 237-342. doi:10.1007/BF00121132
[22] B. R. Oakley, D. R. Kirsch and N. R. Morris, “A Simplified Ultrasensitive Silver Stain for Detecting Proteins in Polyacrylamide Gels,” Analytical Biochemistry, Vol. 105, No. 2, 1980, pp. 361-363. doi:10.1016/0003-2697(80)90470-4
[23] L. V. Thompson, D. Durand, N. A. Fugere and D. A. Ferrington, “Myosin and Actin Expression and Oxidation in Aging Muscle,” Journal of Applied Physiology, Vol. 101, No. 6, 2006, pp. 1581-1587. doi:10.1152/japplphysiol.00426.2006
[24] T. Yamada, T. Mishima, M. Sakamoto, M. Sugiyama, S. Matsunaga and M. Wada, “Oxidation of Myosin Heavy Chain and Reduction in Force Production in Hyperthyroid Rat Soleus,” Journal of Applied Physiology, Vol. 100, No. 5, 2006, pp. 1520-1526. doi:10.1152/japplphysiol.01456.2005
[25] T. G. Favero, D. Colter, P. F. Hooper and J. J. Abramson, “Hypochlorous Acid Inhibits Ca2+-ATPase from Skeletal Muscle Sarcoplasmic Reticulum,” Journal of Applied Physiology, Vol. 84, No. 2, 1998, pp. 425-430.
[26] H. Ohkawa, N. Ohishi and K. Yagi, “Assay for Lipid Peroxides in Animal Tissues by Thiobarbituric Acid Reaction,” Analytical Biochemistry, Vol. 95, No. 2, 1979, pp. 351-358. doi:10.1016/0003-2697(79)90738-3
[27] M. A. Baker, G. J. Cerniglia and A. Zaman, “Microtiter Plate Assay for the Measurement of Glutathione and Glutathione Disulfide in Large Numbers of Biological Samples,” Analytical Biochemistry, Vol. 190, No. 2, 1990, pp. 360-365. doi:10.1016/0003-2697(90)90208-Q
[28] T. Yamada, N. Place, N. Kosterina, T. Ostberg, S. J. Zhang, C. Grundtman, H. Erlandsson-Harris, I. E. Lundberg, B. Glenmark, J. D. Bruton and H. Westerblad, “Impaired Myofibrillar Function in the Soleus Muscle of Mice with Collagen-Induced Arthritis,” Arthritis and Rheumatism, Vol. 60, No. 11, 2009, pp. 3280-3289. doi:10.1002/art.24907
[29] W. B. Kannel and D. L. McGee, “Diabetes and Cardiovascular Disease. The Framingham Study,” The Journal of the American Medical Association, Vol. 241, No. 19, 1979, pp. 2035-2038. doi:10.1001/jama.1979.03290450033020
[30] Y. Tang, C. Gao, M. Xing, Y. Li, L. Zhu, D. Wang, X. Yang, L. Liu and P. Yao, “Quercetin Prevents EthanolInduced Dyslipidemia and Mitochondrial Oxidative Damage,” Food and Chemical Toxicology, Vol. 50, No. 5, 2012, pp. 1194-1200. doi:10.1016/j.fct.2012.02.008
[31] L. Zu, D. Bedja, K. Fox-Talbot, K. L. Gabrielson, L. V. Kaer, L. C. Becker and Z. P. Cai, “Evidence for a Role of Immunoproteasomes in Regulating Cardiac Muscle Mass in Diabetic Mice,” Journal of Molecular and Cellular Cardiology, Vol. 49, No. 1, 2010, pp. 5-15. doi:10.1016/j.yjmcc.2010.02.007
[32] M. Aragno, R. Mastrocola, C. Medana, M. G. Catalano, I. Vercellinatto, O. Danni and G. Boccuzzi, “Oxidative StressDependent Impairment of Cardiac-Specific Transcription Factors in Experimental Diabetes,” Endocrinology, Vol. 147, No. 12, 2006, pp. 5967-5974. doi:10.1210/en.2006-0728
[33] Q. Liang, E. C. Carlson, R. V. Donthi, P. M. Kralik, X. Shen and P. N. Epstein, “Overexpression of Metallothionein Reduces Diabetic Cardiomyopathy,” Diabetes, Vol. 51, No. 1, 2002, pp. 174-181. doi:10.2337/diabetes.51.1.174
[34] D. G. Allen, G. D. Lamb and H. Westerblad, “Skeletal Muscle Fatigue: Cellular Mechanisms,” Physiological Reviews, Vol. 88, No. 1, 2008, pp. 287-332. doi:10.1152/physrev.00015.2007

  
comments powered by Disqus

Copyright © 2018 by authors and Scientific Research Publishing Inc.

Creative Commons License

This work and the related PDF file are licensed under a Creative Commons Attribution 4.0 International License.