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Cardiovascular Toxicology

Erschienen in:

01.04.2015

Antithetical Regulation of α-Myosin Heavy Chain Between Fetal and Adult Heart Failure Though Shuttling of HDAC5 Regulating YY-1 Function

verfasst von: Jie Fang, Yifei Li, Kaiyu Zhou, Yimin Hua, Chuan Wang, Dezhi Mu

Erschienen in: Cardiovascular Toxicology | Ausgabe 2/2015

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Abstract

Molecular switches of myosin isoforms are known to occur in various conditions. Here, we demonstrated the result from fetal heart failure and its potential mechanisms. Fetal and adult heart failure rat models were induced by injections of isoproterenol as previously described, and Go6976 was given to heart failing fetuses. Real-time PCR and Western blot were adopted to measure the expressions of α-MHC, β-MHC and YY-1. Co-immunoprecipitation was performed to analysis whether YY-1 interacts with HDAC5. Besides, histological immunofluorescence assessment was carried out to identify the location of HDAC5. α-MHC was recorded elevated in fetal heart failure which was decreased in adult heart failure. Besides, YY-1 was observed elevated both in fetal and adult failing hearts, but YY-1 could co-immunoprecipitation with HDAC5 only in adult hearts. Nuclear localization of HDAC5 was identified in adult cardiomyocytes, while cytoplasmic localization was identified in fetuses. After Go6976 supplied, HDAC5 shuttled into nucleuses interacted with YY-1. The myosin molecular switches were reversed with worsening cardiac functions and higher mortalities. Regulation of MHC in fetal heart failure was different from adult which provided a better compensation with increased α-MHC. This kind of transition was involved with shuttling of HDAC5 regulating YY-1 function.

Thakur, V., Fouron, J. C., Mertens, L., & Jaeggi, E. T. (2013). Diagnosis and management of fetal heart failure. Canadian Journal of Cardiology, 29, 759–767.CrossRefPubMed

Zhou, K., Hua, Y., Zhu, Q., Liu, H., Yang, S., et al. (2011). Transplacental digoxin therapy for fetal tachyarrhythmia with multiple evaluation systems. Journal of Maternal-Fetal and Neonatal Medicine, 24, 1378–1383.CrossRefPubMed

Zhou, K., Zhou, R., Zhu, Q., Li, Y., Wang, C., et al. (2013). Evaluation of therapeutic effect and cytokine change during transplacental Digoxin treatment for fetal heart failure associated with fetal tachycardia, a case–control study. International Journal of Cardiology, 169, e62–e64.CrossRefPubMed

Zhou, K. Y., Hua, Y. M., & Zhu, Q. (2012). Transplacental digoxin therapy for fetal atrial flutter with hydrops fetalis. World Journal of Pediatrics, 8, 275–277.CrossRefPubMed

Huhta, J. C. (2005). Fetal congestive heart failure. Seminars in Fetal and Neonatal Medicine, 10, 542–552.CrossRefPubMed

Huhta, J. C., & Paul, J. J. (2010). Doppler in fetal heart failure. Clinical Obstetrics and Gynecology, 53, 915–929.CrossRefPubMed

James, J., Martin, L., Krenz, M., Quatman, C., Jones, F., et al. (2005). Forced expression of alpha-myosin heavy chain in the rabbit ventricle results in cardioprotection under cardiomyopathic conditions. Circulation, 111, 2339–2346.CrossRefPubMedCentralPubMed

van Rooij, E., Sutherland, L. B., Qi, X., Richardson, J. A., Hill, J., et al. (2007). Control of stress-dependent cardiac growth and gene expression by a microRNA. Science, 316, 575–579.CrossRefPubMed

Rajabi, M., Kassiotis, C., Razeghi, P., & Taegtmeyer, H. (2007). Return to the fetal gene program protects the stressed heart: A strong hypothesis. Heart Failure Reviews, 12, 331–343.CrossRefPubMed

10.

Taegtmeyer, H., Sen, S., & Vela, D. (2010). Return to the fetal gene program: A suggested metabolic link to gene expression in the heart. Annals of the New York Academy of Sciences, 1188, 191–198.CrossRefPubMedCentralPubMed

11.

Lowes, B. D., Minobe, W., Abraham, W. T., Rizeq, M. N., Bohlmeyer, T. J., et al. (1997). Changes in gene expression in the intact human heart. Downregulation of alpha-myosin heavy chain in hypertrophied, failing ventricular myocardium. Journal of Clinical Investigation, 100, 2315–2324.CrossRefPubMedCentralPubMed

12.

Miyata, S., Minobe, W., Bristow, M. R., & Leinwand, L. A. (2000). Myosin heavy chain isoform expression in the failing and nonfailing human heart. Circulation Research, 86, 386–390.CrossRefPubMed

13.

Li, Y., Fang, J., Hua, Y., Wang, C., Mu, D., et al. (2014). The study of fetal rat model of intra-amniotic isoproterenol injection induced heart dysfunction and phenotypic switch of contractile proteins. BioMed Research International, 2014, 14.CrossRef

14.

Akazawa, H., & Komuro, I. (2003). Roles of cardiac transcription factors in cardiac hypertrophy. Circulation Research, 92, 1079–1088.CrossRefPubMed

15.

Sucharov, C. C., Mariner, P., Long, C., Bristow, M., & Leinwand, L. (2003). Yin Yang 1 is increased in human heart failure and represses the activity of the human alpha-myosin heavy chain promoter. Journal of Biological Chemistry, 278, 31233–31239.CrossRefPubMed

16.

Sucharov, C. C., Langer, S., Bristow, M., & Leinwand, L. (2006). Shuttling of HDAC5 in H9C2 cells regulates YY1 function through CaMKIV/PKD and PP2A. American Journal of Physiology. Cell Physiology, 291, C1029–C1037.CrossRefPubMed

17.

Li, Y., Fang, J., Zhou, K., Wang, C., Mu, D., et al. (2014). Evaluation of oxidative stress in placenta of fetal cardiac dysfunction rat model and antioxidant defenses of maternal vitamin C supplementation with the impacts on P-glycoprotein. Journal of Obstetrics and Gynaecology Research, 40, 1632–1642.CrossRefPubMed

18.

Li, Y., Hua, Y., & Zhou, K. (2014). P-glycoprotein makes no contribution to the lower transplacental transfer of digoxin under fetal heart failure, but who should be blamed for? European Journal of Obstetrics, Gynecology, and Reproductive Biology, 179, 256–257.CrossRefPubMed

19.

Chung, R., Foster, B. K., & Xian, C. J. (2013). Inhibition of protein kinase-D promotes cartilage repair at injured growth plate in rats. Injury, 44, 914–922.CrossRefPubMed

20.

Feng, W., & Li, W. (2010). The study of ISO induced heart failure rat model. Experimental and Molecular Pathology, 88, 299–304.CrossRefPubMed

21.

Mueller, X., Stauffer, J. C., Jaussi, A., Goy, J. J., & Kappenberger, L. (1991). Subjective visual echocardiographic estimate of left ventricular ejection fraction as an alternative to conventional echocardiographic methods: comparison with contrast angiography. Clinical Cardiology, 14, 898–902.CrossRefPubMed

22.

Kleinman, C. S., & Nehgme, R. A. (2004). Cardiac arrhythmias in the human fetus. Pediatric Cardiology, 25, 234–251.CrossRefPubMed

23.

Krenz, M., & Robbins, J. (2004). Impact of beta-myosin heavy chain expression on cardiac function during stress. Journal of the American College of Cardiology, 44, 2390–2397.CrossRefPubMed

24.

Lowes, B. D., Gilbert, E. M., Abraham, W. T., Minobe, W. A., Larrabee, P., et al. (2002). Myocardial gene expression in dilated cardiomyopathy treated with beta-blocking agents. New England Journal of Medicine, 346, 1357–1365.CrossRefPubMed

25.

Bushmeyer, S., Park, K., & Atchison, M. L. (1995). Characterization of functional domains within the multifunctional transcription factor, YY1. Journal of Biological Chemistry, 270, 30213–30220.CrossRefPubMed

26.

Lee, J. S., See, R. H., Galvin, K. M., Wang, J., & Shi, Y. (1995). Functional interactions between YY1 and adenovirus E1A. Nucleic Acids Research, 23, 925–931.CrossRefPubMedCentralPubMed

27.

Bushmeyer, S. M., & Atchison, M. L. (1998). Identification of YY1 sequences necessary for association with the nuclear matrix and for transcriptional repression functions. Journal of Cellular Biochemistry, 68, 484–499.CrossRefPubMed

28.

Lewis, B. A., Tullis, G., Seto, E., Horikoshi, N., Weinmann, R., et al. (1995). Adenovirus E1A proteins interact with the cellular YY1 transcription factor. Journal of Virology, 69, 1628–1636.PubMedCentralPubMed

29.

Yao, Y. L., Yang, W. M., & Seto, E. (2001). Regulation of transcription factor YY1 by acetylation and deacetylation. Molecular and Cellular Biology, 21, 5979–5991.CrossRefPubMedCentralPubMed

30.

Sucharov, C. C., Mariner, P. D., Nunley, K. R., Long, C., Leinwand, L., et al. (2006). A beta1-adrenergic receptor CaM kinase II-dependent pathway mediates cardiac myocyte fetal gene induction. American Journal of Physiology Heart and Circulatory Physiology, 291, H1299–H1308.CrossRefPubMed

31.

Mariner, P. D., Luckey, S. W., Long, C. S., Sucharov, C. C., & Leinwand, L. A. (2005). Yin Yang 1 represses alpha-myosin heavy chain gene expression in pathologic cardiac hypertrophy. Biochemical and Biophysical Research Communications, 326, 79–86.CrossRefPubMed

32.

Hang, C. T., Yang, J., Han, P., Cheng, H. L., Shang, C., et al. (2010). Chromatin regulation by Brg1 underlies heart muscle development and disease. Nature, 466, 62–67.CrossRefPubMedCentralPubMed

33.

McCain, M. L., Sheehy, S. P., Grosberg, A., Goss, J. A., & Parker, K. K. (2013). Recapitulating maladaptive, multiscale remodeling of failing myocardium on a chip. Proceedings of the National Academy of Sciences USA, 110, 9770–9775.CrossRef

Titel: Antithetical Regulation of α-Myosin Heavy Chain Between Fetal and Adult Heart Failure Though Shuttling of HDAC5 Regulating YY-1 Function
verfasst von: Jie Fang
Yifei Li
Kaiyu Zhou
Yimin Hua
Chuan Wang
Dezhi Mu
Publikationsdatum: 01.04.2015
Verlag: Springer US
Erschienen in: Cardiovascular Toxicology / Ausgabe 2/2015
Print ISSN: 1530-7905
Elektronische ISSN: 1559-0259
DOI: https://doi.org/10.1007/s12012-014-9277-8

Springer Medizin

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