Intravenous Semaphorin 3A Administration Maintains Cardiac Contractility and Improves Electrical Remodeling in a Mouse Model of Isoproterenol-Induced Heart Failure

The effects of recombinant semaphorin 3A (Sema3A) on myocardial contractility and electrical remodeling in mice with isoproterenol (ISP) -induced heart failure were investigated.C57BL/6J mice intraperitoneally received ISP (480 mg/kg/day, ISP group; n = 24) or saline (control group; n = 31) for 14 d...

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Published inInternational Heart Journal Vol. 64; no. 3; pp. 453 - 461
Main Authors Kurokawa, Sayaka, Kashimoto, Miwa, Hagikura, Kazuhiro, Shimodai-Yamada, Sayaka, Otsuka, Naoto, Wakamatsu, Yuji, Nagashima, Koichi, Matsumoto, Taro, Hao, Hiroyuki, Okumura, Yasuo
Format Journal Article
LanguageEnglish
Published Japan International Heart Journal Association 31.05.2023
Japan Science and Technology Agency
Subjects
Action potential
Ca2+-transporting ATPase
Cardiac remodeling
Congestive heart failure
Fibrosis
Heart failure
Innervation
Intravenous administration
Isoproterenol
Muscle contraction
Myocardium
Potassium channel
Potassium channels (voltage-gated)
Semaphorins
Sympathetic nervous system
Systolic function
Ventricle
Western blotting
Cardiac remodeling
Sympathetic nervous system
Potassium channel
Systolic function
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Abstract The effects of recombinant semaphorin 3A (Sema3A) on myocardial contractility and electrical remodeling in mice with isoproterenol (ISP) -induced heart failure were investigated.C57BL/6J mice intraperitoneally received ISP (480 mg/kg/day, ISP group; n = 24) or saline (control group; n = 31) for 14 days. Twenty-one ISP-treated mice received 0.5 mg/kg Sema3A intravenously on days 7 and 11 (ISP+Sema3A group). The sympathetic nervous system was activated upon ISP treatment, but was reduced upon Sema3A administration. Greater myocardial tissue fibrosis was observed in the ISP group than in the control group. However, fibrosis was not significantly different between the ISP+Sema3A and control groups. Fractional shortening of the left ventricle was lower in the ISP group than in the control group and was restored in the ISP+Sema3A group (control, 53 ± 8%; ISP, 37 ± 7%; ISP+Sema3A, 48 ± 3%; P < 0.05). Monophasic action potential duration at 20% repolarization (MAPD20) was prolonged in the ISP group (compared to control group), but this was reversed upon Sema3A administration (control, 29 ± 3 ms; ISP, 35 ± 6 ms; ISP+Sema3A, 29 ± 3 ms; P < 0.05). qPCR revealed Kv4.3, KChIP2, and SERCA2 downregulation in the ISP group and upregulation in the ISP+Sema3A group; however, Western blotting revealed similar changes only for Kv4.3 (P < 0.05).Intravenous Sema3A may maintain myocardial contractility by suppressing the sympathetic innervation of the myocardium and reducing myocardial tissue damage, in addition to restoring MAPD via Kv4.3 upregulation.
AbstractList The effects of recombinant semaphorin 3A (Sema3A) on myocardial contractility and electrical remodeling in mice with isoproterenol (ISP) -induced heart failure were investigated.C57BL/6J mice intraperitoneally received ISP (480 mg/kg/day, ISP group; n = 24) or saline (control group; n = 31) for 14 days. Twenty-one ISP-treated mice received 0.5 mg/kg Sema3A intravenously on days 7 and 11 (ISP+Sema3A group). The sympathetic nervous system was activated upon ISP treatment, but was reduced upon Sema3A administration. Greater myocardial tissue fibrosis was observed in the ISP group than in the control group. However, fibrosis was not significantly different between the ISP+Sema3A and control groups. Fractional shortening of the left ventricle was lower in the ISP group than in the control group and was restored in the ISP+Sema3A group (control, 53 ± 8%; ISP, 37 ± 7%; ISP+Sema3A, 48 ± 3%; P < 0.05). Monophasic action potential duration at 20% repolarization (MAPD20) was prolonged in the ISP group (compared to control group), but this was reversed upon Sema3A administration (control, 29 ± 3 ms; ISP, 35 ± 6 ms; ISP+Sema3A, 29 ± 3 ms; P < 0.05). qPCR revealed Kv4.3, KChIP2, and SERCA2 downregulation in the ISP group and upregulation in the ISP+Sema3A group; however, Western blotting revealed similar changes only for Kv4.3 (P < 0.05).Intravenous Sema3A may maintain myocardial contractility by suppressing the sympathetic innervation of the myocardium and reducing myocardial tissue damage, in addition to restoring MAPD via Kv4.3 upregulation.
The effects of recombinant semaphorin 3A (Sema3A) on myocardial contractility and electrical remodeling in mice with isoproterenol (ISP) -induced heart failure were investigated.C57BL/6J mice intraperitoneally received ISP (480 mg/kg/day, ISP group; n = 24) or saline (control group; n = 31) for 14 days. Twenty-one ISP-treated mice received 0.5 mg/kg Sema3A intravenously on days 7 and 11 (ISP+Sema3A group). The sympathetic nervous system was activated upon ISP treatment, but was reduced upon Sema3A administration. Greater myocardial tissue fibrosis was observed in the ISP group than in the control group. However, fibrosis was not significantly different between the ISP+Sema3A and control groups. Fractional shortening of the left ventricle was lower in the ISP group than in the control group and was restored in the ISP+Sema3A group (control, 53 ± 8%; ISP, 37 ± 7%; ISP+Sema3A, 48 ± 3%; P < 0.05). Monophasic action potential duration at 20% repolarization (MAPD ) was prolonged in the ISP group (compared to control group), but this was reversed upon Sema3A administration (control, 29 ± 3 ms; ISP, 35 ± 6 ms; ISP+Sema3A, 29 ± 3 ms; P < 0.05). qPCR revealed Kv4.3, KChIP2, and SERCA2 downregulation in the ISP group and upregulation in the ISP+Sema3A group; however, Western blotting revealed similar changes only for Kv4.3 (P < 0.05).Intravenous Sema3A may maintain myocardial contractility by suppressing the sympathetic innervation of the myocardium and reducing myocardial tissue damage, in addition to restoring MAPD via Kv4.3 upregulation.
ArticleNumber 22-705
Author Hao, Hiroyuki
Okumura, Yasuo
Shimodai-Yamada, Sayaka
Kashimoto, Miwa
Wakamatsu, Yuji
Hagikura, Kazuhiro
Kurokawa, Sayaka
Matsumoto, Taro
Otsuka, Naoto
Nagashima, Koichi
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  fullname: Hagikura, Kazuhiro
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  fullname: Shimodai-Yamada, Sayaka
  organization: Division of Human Pathology, Department of Pathology and Microbiology, Nihon University School of Medicine
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  fullname: Otsuka, Naoto
  organization: Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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  fullname: Wakamatsu, Yuji
  organization: Division of Cardiology, Department of Medicine, Nihon University School of Medicine
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Cites_doi 10.1038/nrcardio.2011.139
10.1016/j.yjmcc.2020.08.001
10.1016/S0008-6363(98)00135-7
10.3949/ccjm.75.Suppl_2.S94
10.1253/circj.CJ-10-1089
10.1152/ajpheart.00508.2010
10.1074/jbc.M114.582809
10.1161/01.RES.0000269828.62250.ab
10.1007/s11427-011-4183-9
10.1016/j.bbrc.2014.04.157
10.1161/CIRCRESAHA.115.303657
10.1371/journal.pgen.1003364
10.1007/s00395-017-0630-5
10.1016/S0079-6123(08)64012-1
10.1016/j.jacc.2009.03.061
10.1111/1440-1681.12176
10.1254/jjp.82.273
10.1038/nm1570
10.1038/jid.2008.150
10.4149/gpb_2012_015
10.1161/01.RES.0000133678.22968.e3
10.1038/nature11000
10.1620/tjem.225.51
10.1253/circj.CJ-13-1587
10.1002/humu.23730
10.1016/S0092-8674(03)00267-8
10.1186/s12872-016-0192-8
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References 23. Zhou S, Chen LS, Miyauchi Y, et al. Mechanisms of cardiac nerve sprouting after myocardial infarction in dogs. Circ Res 2004; 95: 76-83.
20. Yoshida T, Yamashita M, Horimai C, Hayashi M. Kruppel-like factor 4 protein regulates isoproterenol-induced cardiac hypertrophy by modulating myocardin expression and activity. J Biol Chem 2014; 289: 26107-18.
4. Kolodkin AL. Semaphorin-mediated neuronal growth cone guidance. Prog Brain Res 1998; 117: 115-32.
17. Horiuchi-Hirose M, Kashihara T, Nakada T, et al. Decrease in the density of t-tubular L-type Ca2+ channel currents in failing ventricular myocytes. Am J Physiol Heart Circ Physiol 2011; 300: H978-88.
27. Rienks M, Carai P, Bitsch N, et al. Sema3A promotes the resolution of cardiac inflammation after myocardial infarction. Basic Res Cardiol 2017; 112: 42.
28. Hu H, Xuan Y, Xue M, et al. Semaphorin 3A attenuates cardiac autonomic disorders and reduces inducible ventricular arrhythmias in rats with experimental myocardial infarction. BMC Cardiovasc Disord 2016; 16: 16.
1. Zipes DP. Heart-brain interactions in cardiac arrhythmias: role of the autonomic nervous system. Cleve Clin J Med 2008; 75: S94-6.
26. Campuzano O, Sarquella-Brugada G, Fernandez-Falgueras A, et al. Genetic interpretation and clinical translation of minor genes related to Brugada syndrome. Hum Mutat 2019; 40: 749-64.
13. Wen HZ, Jiang H, Li L, et al. Semaphorin 3A attenuates electrical remodeling at infarct border zones in rats after myocardial infarction. Tohoku J Exp Med 2011; 225: 51-7.
3. Floras JS. Sympathetic nervous system activation in human heart failure: clinical implications of an updated model. J Am Coll Cardiol 2009; 54: 375-85.
10. Hayashi M, Nakashima T, Taniguchi M, Kodama T, Kumanogoh A, Takayanagi H. Osteoprotection by semaphorin 3A. Nature 2012; 485: 69-74.
24. Kimura K, Ieda M, Kanazawa H, et al. Cardiac sympathetic rejuvenation: A link between nerve function and cardiac hypertrophy. Circ Res 2007; 100: 1755-64.
12. Boczek NJ, Ye D, Johnson EK, et al. Characterization of SEMA3A-encoded semaphorin as a naturally occurring Kv4.3 protein inhibitor and its contribution to Brugada syndrome. Circ Res 2014; 115: 460-9.
5. Goshima Y, Sasaki Y, Nakayama T, Ito T, Kimura T. Functions of semaphorins in axon guidance and neuronal regeneration. Jpn J Pharmacol 2000; 82: 273-9.
11. Yamaguchi J, Nakamura F, Aihara M, et al. Semaphorin3A alleviates skin lesions and scratching behavior in NC/Nga mice, an atopic dermatitis model. J Invest Dermatol 2008; 128: 2842-9.
8. Narematsu M, Kamimura T, Yamagishi T, Nakajima Y. Hypoxia-induced downregulation of Sema3a and CXCL12/CXCR4 regulate the formation of the coronary artery stem at the proper site. J Mol Cell Cardiol 2020; 147: 62-73.
25. Nakano Y, Chayama K, Ochi H, et al. A nonsynonymous polymorphism in semaphorin 3A as a risk factor for human unexplained cardiac arrest with documented ventricular fibrillation. PLoS Genet 2013; 9: e1003364.
19. Liu L, Cui J, Yang Q, et al. Apocynin attenuates isoproterenol-induced myocardial injury and fibrogenesis. Biochem Biophys Res Commun 2014; 449: 55-61.
22. Nishiyama A, Kambe F, Kamiya K, Seo H, Toyama J. Effects of thyroid status on expression of voltage-gated potassium channels in rat left ventricle. Cardiovasc Res 1998; 40: 343-51.
6. Bagri A, Cheng HJ, Yaron A, Pleasure SJ, Tessier-Lavigne M. Stereotyped pruning of long hippocampal axon branches triggered by retraction inducers of the semaphorin family. Cell 2003; 113: 285-99.
9. Sun SQ, Wang XT, Qu XF, et al. Increased expression of myocardial semaphorin 3A in isoproterenol-induced heart failure rats. Chin Med J (Engl) 2011; 124: 2173-8.
14. Kurokawa S, Niwano S, Niwano H, et al. Cardiomyocyte-derived mitochondrial superoxide causes myocardial electrical remodeling by downregulating potassium channels and related molecules. Circ J 2014; 78: 1950-9.
16. Nichtova Z, Novotova M, Kralova E, Stankovicova T. Morphological and functional characteristics of models of experimental myocardial injury induced by isoproterenol. Gen Physiol Biophys 2012; 31: 141-51.
21. Li H, Lu ZZ, Chen C, Song Y, Xiao H, Zhang YY. Echocardiographic assessment of beta-adrenoceptor stimulation-induced heart failure with reduced heart rate in mice. Clin Exp Pharmacol Physiol 2014; 41: 58-66.
7. Ieda M, Kanazawa H, Kimura K, et al. Sema3a maintains normal heart rhythm through sympathetic innervation patterning. Nat Med 2007; 13: 604-12.
2. Shen MJ, Choi EK, Tan AY, et al. Neural mechanisms of atrial arrhythmias. Nat Rev Cardiol 2011; 9: 30-9.
15. Kurokawa S, Niwano S, Niwano H, et al. Progression of ventricular remodeling and arrhythmia in the primary hyperoxidative state of glutathione-depleted rats. Circ J 2011; 75: 1386-93.
18. Ma X, Song Y, Chen C, et al. Distinct actions of intermittent and sustained beta-adrenoceptor stimulation on cardiac remodeling. Sci China Life Sci 2011; 54: 493-501.
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23
24
25
26
27
28
10
11
12
13
14
15
16
17
18
19
1
2
3
4
5
6
7
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20
21
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  doi: 10.1038/nrcardio.2011.139
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  doi: 10.1016/S0008-6363(98)00135-7
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  doi: 10.3949/ccjm.75.Suppl_2.S94
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  doi: 10.1253/circj.CJ-10-1089
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  doi: 10.1152/ajpheart.00508.2010
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  doi: 10.1074/jbc.M114.582809
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  doi: 10.1161/01.RES.0000269828.62250.ab
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  doi: 10.1007/s11427-011-4183-9
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  doi: 10.1016/j.bbrc.2014.04.157
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  doi: 10.1161/CIRCRESAHA.115.303657
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  doi: 10.1371/journal.pgen.1003364
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  doi: 10.1007/s00395-017-0630-5
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  doi: 10.1016/S0079-6123(08)64012-1
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  doi: 10.1016/j.jacc.2009.03.061
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  doi: 10.1111/1440-1681.12176
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  doi: 10.1254/jjp.82.273
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  doi: 10.1038/nm1570
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  doi: 10.1038/jid.2008.150
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  doi: 10.4149/gpb_2012_015
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  doi: 10.1161/01.RES.0000133678.22968.e3
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  doi: 10.1038/nature11000
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  doi: 10.1620/tjem.225.51
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  doi: 10.1253/circj.CJ-13-1587
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  doi: 10.1002/humu.23730
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Snippet The effects of recombinant semaphorin 3A (Sema3A) on myocardial contractility and electrical remodeling in mice with isoproterenol (ISP) -induced heart failure...
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SubjectTerms Action potential
Ca2+-transporting ATPase
Cardiac remodeling
Congestive heart failure
Fibrosis
Heart failure
Innervation
Intravenous administration
Isoproterenol
Muscle contraction
Myocardium
Potassium channel
Potassium channels (voltage-gated)
Semaphorins
Sympathetic nervous system
Systolic function
Ventricle
Western blotting
Title Intravenous Semaphorin 3A Administration Maintains Cardiac Contractility and Improves Electrical Remodeling in a Mouse Model of Isoproterenol-Induced Heart Failure
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