| Autor: |
Shioura K; Department of Medicine/Section of Cardiology, University of Illinois, Chicago, Illinois, USA., Pena J; Department of Physiology & Cardiovascular Center, Medical College of Wisconsin, Milwaukee, USA., Goldspink P; Department of Physiology & Cardiovascular Center, Medical College of Wisconsin, Milwaukee, USA. |
| Jazyk: |
angličtina |
| Zdroj: |
International journal of cardiovascular research [Int J Cardiovasc Res] 2014 Jun 24; Vol. 3 (3), pp. 1000169. |
| DOI: |
10.4172/2324-8602.1000169 |
| Abstrakt: |
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. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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