HGF Overexpression in Myoblast Sheets Enhances Angiogenesis in Heart Failure Rats
Author Information
Author(s): Siltanen Antti, Kitabayashi Katsukiyo, Lakkisto Päivi, Mäkelä Johanna, Pätilä Tommi, Ono Masamichi, Tikkanen Ilkka, Sawa Yoshiki, Kankuri Esko, Harjula Ari
Primary Institution: Institute of Biomedicine, University of Helsinki, Helsinki, Finland
Hypothesis
We hypothesized that in a rat model of MI-induced chronic heart failure, myoblast sheet therapy could be improved by overexpression of hepatocyte growth factor (HGF).
Conclusion
L6-HGF therapy effectively induced angiogenesis in the chronically failing heart, but cardiac function was not further enhanced by hHGF expression.
Supporting Evidence
- Paracrine mediators from L6-HGF myoblast sheets effectively induced migration of cardiac endothelial and smooth muscle cells.
- L6-HGF therapy induced a significant increase in SMA-positive and vWF-positive tissue compared to control and L6-WT groups.
- Both L6-WT and L6-HGF therapies enhanced cardiac function and inhibited remodeling in a similar fashion.
Takeaway
Researchers wanted to see if adding a special growth factor to muscle cells could help heal hearts better after damage. They found that while it helped blood vessels grow, it didn't make the heart work better.
Methodology
The study involved inducing myocardial infarction in Wistar rats, followed by treatment with either wild type or HGF-expressing myoblast sheets, and evaluating cardiac function and angiogenesis.
Potential Biases
Potential bias in the selection of treatment groups and the assessment of outcomes.
Limitations
The study did not assess the long-term effects of HGF therapy on cardiac function beyond 4 weeks.
Participant Demographics
Wistar rats, 250–400 g.
Statistical Information
P-Value
p<0.05
Statistical Significance
p<0.05
Digital Object Identifier (DOI)
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