scholarly journals Isoform-Specific Modulation of Inflammation Induced by Adenoviral Mediated Delivery of Platelet-Derived Growth Factors in the Adult Mouse Heart

PLoS ONE ◽  
2016 ◽  
Vol 11 (8) ◽  
pp. e0160930 ◽  
Author(s):  
Radiosa Gallini ◽  
Jenni Huusko ◽  
Seppo Ylä-Herttuala ◽  
Christer Betsholtz ◽  
Johanna Andrae
2007 ◽  
Vol 282 (33) ◽  
pp. 24057-24064 ◽  
Author(s):  
Maike Krenz ◽  
Sakthivel Sadayappan ◽  
Hanna E. Osinska ◽  
Jeffrey A. Henry ◽  
Samantha Beck ◽  
...  

2013 ◽  
Vol 5 (2) ◽  
pp. 191-209 ◽  
Author(s):  
Konstantinos Malliaras ◽  
Yiqiang Zhang ◽  
Jeffrey Seinfeld ◽  
Giselle Galang ◽  
Eleni Tseliou ◽  
...  

Stem Cells ◽  
2006 ◽  
Vol 24 (7) ◽  
pp. 1738-1749 ◽  
Author(s):  
Malancha Ta ◽  
Yong Choi ◽  
Fouad Atouf ◽  
Cheol Hong Park ◽  
Nadya Lumelsky

Circulation ◽  
2011 ◽  
Vol 123 (5) ◽  
pp. 504-514 ◽  
Author(s):  
Mortimer Korf-Klingebiel ◽  
Tibor Kempf ◽  
Klaus-Dieter Schlüter ◽  
Christian Willenbockel ◽  
Torben Brod ◽  
...  

2016 ◽  
Vol 2 (11) ◽  
pp. e1600844 ◽  
Author(s):  
William C. W. Chen ◽  
Zhouguang Wang ◽  
Maria Azzurra Missinato ◽  
Dae Woo Park ◽  
Daniel Ward Long ◽  
...  

Heart attack is a global health problem that leads to significant morbidity, mortality, and health care burden. Adult human hearts have very limited regenerative capability after injury. However, evolutionarily primitive species generally have higher regenerative capacity than mammals. The extracellular matrix (ECM) may contribute to this difference. Mammalian cardiac ECM may not be optimally inductive for cardiac regeneration because of the fibrotic, instead of regenerative, responses in injured adult mammalian hearts. Given the high regenerative capacity of adult zebrafish hearts, we hypothesize that decellularized zebrafish cardiac ECM (zECM) made from normal or healing hearts can induce mammalian heart regeneration. Using zebrafish and mice as representative species of lower vertebrates and mammals, we show that a single administration of zECM, particularly the healing variety, enables cardiac functional recovery and regeneration of adult mouse heart tissues after acute myocardial infarction. zECM-treated groups exhibit proliferation of the remaining cardiomyocytes and multiple cardiac precursor cell populations and reactivation of ErbB2 expression in cardiomyocytes. Furthermore, zECM exhibits pro-proliferative and chemotactic effects on human cardiac precursor cell populations in vitro. These contribute to the structural preservation and correlate with significantly higher cardiac contractile function, notably less left ventricular dilatation, and substantially more elastic myocardium in zECM-treated hearts than control animals treated with saline or decellularized adult mouse cardiac ECM. Inhibition of ErbB2 activity abrogates beneficial effects of zECM administration, indicating the possible involvement of ErbB2 signaling in zECM-mediated regeneration. This study departs from conventional focuses on mammalian ECM and introduces a new approach for cardiac tissue regeneration.


Gene ◽  
2019 ◽  
Vol 697 ◽  
pp. 40-47
Author(s):  
Xia Huang ◽  
Ziyi Li ◽  
Jisheng Hu ◽  
Zihao Yang ◽  
Zhongying Liu ◽  
...  

2000 ◽  
Vol 278 (2) ◽  
pp. H412-H419 ◽  
Author(s):  
Jil C. Tardiff ◽  
Timothy E. Hewett ◽  
Stephen M. Factor ◽  
Karen L. Vikstrom ◽  
Jeffrey Robbins ◽  
...  

α- and β-myosin heavy chain (MHC), the two MHC isoforms expressed in the mammalian heart, differ quantitatively in their enzymatic activities. The MHC composition of the heart can change dramatically in response to numerous stimuli, leading to the hypothesis that changes in cardiac function can be caused by myosin isoform shifts. However, this hypothesis has remained unproven because the stimuli used to generate these shifts are complex and accompanied by many additional physiological changes, including alterations in cardiac mass and geometry. Adult mouse ventricles normally express only α-MHC (the faster motor). To determine whether genetic alteration of the MHC isoform composition in the adult mouse heart would result in changes in cardiac chamber mass and contractility, we established transgenic mouse lines that express a Myc-tagged β-MHC molecule (the slower motor) in adult ventricular tissue, one of which expreses 12% of its myosin as the transgene. There is no evidence of hypertrophy, induction of hypertrophic markers, and no histopathology. Myofibrillar Ca2+-activated ATPase activity is decreased by 23%, and Langendorff preparations demonstrate a significant 15% decrease in systolic function in transgenic hearts. These results suggest that even small shifts in the myosin isoform composition of the myocardium can result in physiologically significant changes in cardiac contractility and could be relevant to cardiovascular disease.


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