Enhancing Repair of the Mammalian Heart.
From: European Molecular Biology Laboratory, Mouse Biology Unit Monterotondo, Rome, Italy.
Circulation research
- Publish Date: Jun 2007
- ISSN: 1524-4571
- Volume: 100
- Issue: 12
- Pages: 1732-40
- Medium: Internet
- Language: English
- Citation (JAMA): Santini Maria Paola, Tsao Lana, Monassier Laurent, et al. Enhancing Repair of the Mammalian Heart.. Circ. Res. Jun 2007;100:1732-40
Abstract
The injured mammalian heart is particularly susceptible to tissue deterioration, scarring, and loss of contractile function in response to trauma or sustained disease. We tested the ability of a locally acting insulin-like growth factor-1 isoform (mIGF-1) to recover heart functionality, expressing the transgene in the mouse myocardium to exclude endocrine effects on other tissues. supplemental mIGF-1 expression did not perturb normal cardiac growth and physiology. Restoration of cardiac function in post-infarct mIGF-1 transgenic mice was facilitated by modulation of the inflammatory response and increased antiapoptotic signaling. mIGF-1 ventricular tissue exhibited increased proliferative activity several weeks after injury. The canonical signaling pathway involving Akt, mTOR, and p70S6 kinase was not induced in mIGF-1 hearts, which instead activated alternate PDK1 and SGK1 signaling intermediates. The robust response achieved with the mIGF-1 isoform provides a mechanistic basis for clinically feasible therapeutic strategies for improving the outcome of heart disease.
Mesh Headings (Keywords): Animals, Cell Proliferation, Cells, Cultured, Cicatrix, DNA, Complementary, Gene Expression Regulation, Inflammation, Insulin-Like Growth Factor I, Mice, Mice, Transgenic, Myocardial Contraction, Myocardial Infarction, Myocytes, Cardiac, Protein Isoforms, Recovery of Function, Signal Transduction, Wound Healing
Check for Full Text / PubMed Unique Identifier (PMID): 17525368
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