Display options
Cite
Shioura K, Pena J, Goldspink P. Administration of a Synthetic Peptide Derived from the E-domain Region of Mechano-Growth Factor Delays Decompensation Following Myocardial Infarction. Int J Cardiovasc Res. 2014;3(3):1000169doi: 10.4172/2324-8602.1000169.
Shioura, K., Pena, J., & Goldspink, P. (2014). Administration of a Synthetic Peptide Derived from the E-domain Region of Mechano-Growth Factor Delays Decompensation Following Myocardial Infarction. International journal of cardiovascular research, 3(3), 1000169. https://doi.org/10.4172/2324-8602.1000169
Shioura, Km, et al. "Administration of a Synthetic Peptide Derived from the E-domain Region of Mechano-Growth Factor Delays Decompensation Following Myocardial Infarction." International journal of cardiovascular research vol. 3,3 (2014): 1000169. doi: https://doi.org/10.4172/2324-8602.1000169
Shioura K, Pena J, Goldspink P. Administration of a Synthetic Peptide Derived from the E-domain Region of Mechano-Growth Factor Delays Decompensation Following Myocardial Infarction. Int J Cardiovasc Res. 2014 Jun 24;3(3):1000169. doi: 10.4172/2324-8602.1000169. PMID: 25606570; PMCID: PMC4297642.
Copy Download .nbib Format: NLM
Share it on

Int J Cardiovasc Res. 2014 Jun 24;3(3):1000169. doi: 10.4172/2324-8602.1000169.

Administration of a Synthetic Peptide Derived from the E-domain Region of Mechano-Growth Factor Delays Decompensation Following Myocardial Infarction.

International journal of cardiovascular research

Km Shioura, Jr Pena, Ph Goldspink

Affiliations

  1. Department of Medicine/Section of Cardiology, University of Illinois, Chicago, Illinois, USA.
  2. Department of Physiology & Cardiovascular Center, Medical College of Wisconsin, Milwaukee, USA.

PMID: 25606570 PMCID: PMC4297642 DOI: 10.4172/2324-8602.1000169

Abstract

Insulin like growth factor-I (IGF-1) isoforms differ structurally in their E-domain regions and their temporal expression profile in response to injury. We and others have reported that Mechano-growth factor (MGF), which is equivalent to human IGF-1c and rodent IGF-1Eb isoforms, is expressed acutely following myocardial infarction (MI) in the mouse heart. To examine the function of the E-domain region, we have used a stabilized synthetic peptide analog corresponding to the unique 24 amino acid region E-domain of MGF. Here we deliver the human MGF E-domain peptide to mice during the acute phase (within 12 hours) and the chronic phase (8 weeks) post-MI. We assessed the impact of peptide delivery on cardiac function and cardiovascular hemodynamics by pressure-volume (P-V) loop analysis and gene expression by quantitative RT-PCR. A significant decline in both systolic and diastolic hemodynamics accompanied by pathologic hypertrophy occurred by 10 weeks post-MI in the untreated group. Delivery of the E-domain peptide during the acute phase post-MI ameliorated the decline in hemodynamics, delayed decompensation but did not prevent pathologic hypertrophy. Delivery during the chronic phase post-MI significantly improved systolic function, predominantly due to the effects on vascular resistance and prevented decompensation. While pathologic hypertrophy persisted there was a significant decline in atrial natriuretic factor (ANF) expression in the E-domain peptide treated hearts. Taken together our data suggest that administration of the MGF E-domain peptide derived from the propeptide form of IGF-1Ec may be used to facilitate the actions of IGF-I produced by the tissue during the progression of heart failure to improve cardiovascular function.

Keywords: Cardiovascular function; E-domain; IGF-1 isoforms; Myocardial Infarction

References

  1. Am J Physiol Heart Circ Physiol. 2001 Jun;280(6):H2902-10 - PubMed
  2. Lancet. 1998 Apr 25;351(9111):1233-7 - PubMed
  3. Annu Rev Physiol. 1985;47:443-67 - PubMed
  4. PLoS One. 2012;7(12):e51152 - PubMed
  5. J Physiol. 2003 Jun 1;549(Pt 2):409-18 - PubMed
  6. Proc Soc Exp Biol Med. 1996 Nov;213(2):187-92 - PubMed
  7. In Vivo. 2009 Jul-Aug;23(4):567-75 - PubMed
  8. Am J Physiol Heart Circ Physiol. 2007 Nov;293(5):H2870-7 - PubMed
  9. Circulation. 2002 Aug 20;106(8):939-44 - PubMed
  10. Heart Lung Circ. 2008 Feb;17 (1):33-9 - PubMed
  11. Curr Biol. 1999 Jul 29-Aug 12;9(15):845-8 - PubMed
  12. J Neurosci Res. 2011 Mar;89(3):394-405 - PubMed
  13. J Appl Physiol (1985). 2010 May;108(5):1069-76 - PubMed
  14. Am J Physiol. 1983 Feb;244(2):H206-14 - PubMed
  15. Eur Heart J. 1992 Nov;13 Suppl E:85-90 - PubMed
  16. Am J Physiol Regul Integr Comp Physiol. 2008 Aug;295(2):R528-34 - PubMed
  17. Int J Cardiol. 2003 Feb;87(2-3):185-91 - PubMed
  18. Circulation. 2000 Apr 4;101(13):1539-45 - PubMed
  19. Circ Res. 2002 Jun 14;90(11):1205-13 - PubMed
  20. Circ Res. 1998 Jul 13;83(1):50-9 - PubMed
  21. Am J Physiol. 1979 Mar;236(3):H498-505 - PubMed
  22. J Biol Chem. 1997 Mar 7;272(10):6663-70 - PubMed
  23. Am J Physiol. 1994 Jun;266(6 Pt 2):H2468-75 - PubMed
  24. Am J Physiol. 1979 Mar;236(3):H494-7 - PubMed
  25. J Clin Invest. 1995 Feb;95(2):619-27 - PubMed
  26. J Clin Invest. 1996 Dec 1;98(11):2648-55 - PubMed
  27. J Biol Chem. 1987 Jun 5;262(16):7894-900 - PubMed
  28. FASEB J. 2005 Nov;19(13):1896-8 - PubMed
  29. Endocrinology. 1985 Jun;116(6):2563-7 - PubMed
  30. Endocrine. 2002 Dec;19(3):287-92 - PubMed
  31. Eur J Heart Fail. 2010 Nov;12(11):1214-22 - PubMed
  32. PLoS One. 2012;7(9):e45588 - PubMed
  33. Proc Natl Acad Sci U S A. 1992 Sep 1;89(17):8107-11 - PubMed
  34. Mol Cell Biochem. 2013 Sep;381(1-2):69-83 - PubMed
  35. J Biol Chem. 1991 Apr 15;266(11):7300-5 - PubMed
  36. J Am Coll Cardiol. 2001 Jul;38(1):26-32 - PubMed
  37. Heart Lung Circ. 2005 Jun;14(2):98-103 - PubMed
  38. Endocrinology. 2002 Nov;143(11):4235-42 - PubMed
  39. Endocrinology. 2013 Mar;154(3):1215-24 - PubMed
  40. Circulation. 1996 Jun 15;93(12):2188-96 - PubMed
  41. Eur Heart J. 1998 Nov;19(11):1704-11 - PubMed
  42. J Clin Invest. 1986 Jun;77(6):1903-8 - PubMed

Publication Types

Grant support