Anti-remodeling and anti-fibrotic effects of the neuregulin-1β glial growth factor 2 in a large animal model of heart failure. Galindo, C. L., Kasasbeh, E., Murphy, A., Ryzhov, S., Lenihan, S., Ahmad, F. A., Williams, P., Nunnally, A., Adcock, J., Song, Y., Harrell, F. E., Tran, T. L., Parry, T. J., Iaci, J., Ganguly, A., Feoktistov, I., Stephenson, M. K., Caggiano, A. O., Sawyer, D. B., & Cleator, J. H. Journal of the American Heart Association, October, 2014.
Anti-remodeling and anti-fibrotic effects of the neuregulin-1β glial growth factor 2 in a large animal model of heart failure. [link]Paper  abstract   bibtex   
Neuregulin-1β (NRG-1β) is a growth factor critical for cardiac development and repair with therapeutic potential for heart failure. We previously showed that the glial growth factor 2 (GGF2) isoform of NRG-1β improves cardiac function in rodents after myocardial infarction (MI), but its efficacy in a large animal model of cardiac injury has not been examined. We therefore sought to examine the effects of GGF2 on ventricular remodeling, cardiac function, and global transcription in post-MI swine, as well as potential mechanisms for anti-remodeling effects. MI was induced in anesthetized swine (n=23) by intracoronary balloon occlusion. At 1 week post-MI, survivors (n=13) received GGF2 treatment (intravenous, biweekly for 4 weeks; n=8) or were untreated (n=5). At 5 weeks post-MI, fractional shortening was higher (32.8% versus 25.3%, P=0.019), and left ventricular (LV) end-diastolic dimension lower (4.5 versus 5.3 cm, P=0.003) in GGF2-treated animals. Treatment altered expression of 528 genes, as measured by microarrays, including collagens, basal lamina components, and matricellular proteins. GGF2-treated pigs exhibited improvements in LV cardiomyocyte mitochondria and intercalated disk structures and showed less fibrosis, altered matrix structure, and fewer myofibroblasts (myoFbs), based on trichrome staining, electron microscopy, and immunostaining. In vitro experiments with isolated murine and rat cardiac fibroblasts demonstrate that NRG-1β reduces myoFbs, and suppresses TGFβ-induced phospho-SMAD3 as well as αSMA expression. These results suggest that GGF2/NRG-1β prevents adverse remodeling after injury in part via anti-fibrotic effects in the heart. o̧pyright 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.
@article{gal14ant,
    abstract = {{Neuregulin-1β (NRG-1β) is a growth factor critical for cardiac development and repair with therapeutic potential for heart failure. We previously showed that the glial growth factor 2 (GGF2) isoform of NRG-1β improves cardiac function in rodents after myocardial infarction (MI), but its efficacy in a large animal model of cardiac injury has not been examined. We therefore sought to examine the effects of GGF2 on ventricular remodeling, cardiac function, and global transcription in post-MI swine, as well as potential mechanisms for anti-remodeling effects. MI was induced in anesthetized swine (n=23) by intracoronary balloon occlusion. At 1 week post-MI, survivors (n=13) received GGF2 treatment (intravenous, biweekly for 4 weeks; n=8) or were untreated (n=5). At 5 weeks post-MI, fractional shortening was higher (32.8\% versus 25.3\%, P=0.019), and left ventricular (LV) end-diastolic dimension lower (4.5 versus 5.3 cm, P=0.003) in GGF2-treated animals. Treatment altered expression of 528 genes, as measured by microarrays, including collagens, basal lamina components, and matricellular proteins. GGF2-treated pigs exhibited improvements in LV cardiomyocyte mitochondria and intercalated disk structures and showed less fibrosis, altered matrix structure, and fewer myofibroblasts (myoFbs), based on trichrome staining, electron microscopy, and immunostaining. In vitro experiments with isolated murine and rat cardiac fibroblasts demonstrate that NRG-1β reduces myoFbs, and suppresses TGFβ-induced phospho-SMAD3 as well as αSMA expression. These results suggest that GGF2/NRG-1β prevents adverse remodeling after injury in part via anti-fibrotic effects in the heart. {\copyright} 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.}},
    author = {Galindo, Cristi L. and Kasasbeh, Ehab and Murphy, Abigail and Ryzhov, Sergey and Lenihan, Sean and Ahmad, Farhaan A. and Williams, Philip and Nunnally, Amy and Adcock, Jamie and Song, Yanna and Harrell, Frank E. and Tran, Truc-Linh L. and Parry, Tom J. and Iaci, Jen and Ganguly, Anindita and Feoktistov, Igor and Stephenson, Matthew K. and Caggiano, Anthony O. and Sawyer, Douglas B. and Cleator, John H.},
    citeulike-article-id = {13416177},
    citeulike-linkout-0 = {http://dx.doi.org/10.1161/JAHA.113.000773},
    citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/25341890},
    citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=25341890},
    
    issn = {2047-9980},
    journal = {Journal of the American Heart Association},
    keywords = {collaboration, cv},
    month = oct,
    number = {5},
    pmid = {25341890},
    posted-at = {2014-11-02 22:57:44},
    priority = {0},
    title = {{Anti-remodeling and anti-fibrotic effects of the neuregulin-1β glial growth factor 2 in a large animal model of heart failure.}},
    url = {http://dx.doi.org/10.1161/JAHA.113.000773},
    volume = {3},
    year = {2014}
}
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