Daniel A. Brenner
Boston University
12 Papers
44 Citations
Daniel A. Brenner is an academic researcher from Boston University. The author has contributed to research in topics: Physical exercise & Oxidative stress. The author has an hindex of 9, co-authored 12 publications.
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Papers
Human amyloidogenic light chains directly impair cardiomyocyte function through an increase in cellular oxidant stress.
Daniel A. Brenner,Mohit Jain,David R. Pimentel,Bo Wang,Lawreen H. Connors,Martha Skinner,Carl S. Apstein,Ronglih Liao +7 more
TL;DR: It is suggested that cardiac dysfunction in amyloid cardiomyopathy is directly mediated by LC protein-inducedCardiomyocyte oxidant stress and alterations in cellular redox status, independent of fibril deposition, and antioxidants or treatment strategies aimed at eliminating circulating LC proteins may therefore be beneficial in the treatment of this fatal disease.
433
Cell Therapy Attenuates Deleterious Ventricular Remodeling and Improves Cardiac Performance After Myocardial Infarction
Mohit Jain,Harout Dersimonian,Daniel A. Brenner,Soeun Ngoy,Paige Teller,Albert S.B. Edge,Agatha Zawadzka,Kristie Wetzel,Douglas B. Sawyer,Wilson S. Colucci,Carl S. Apstein,Ronglih Liao +11 more
TL;DR: Implanted skeletal myoblasts form viable grafts in infarcted myocardium, resulting in enhanced post-MI exercise capacity and contractile function and attenuated ventricular dilation, illustrating that syngeneic myoblast implants after MI improves both in vivo and ex vivo indexes of global ventricular dysfunction and deleterious remodeling.
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Amyloidogenic light chains induce cardiomyocyte contractile dysfunction and apoptosis via a non-canonical p38α MAPK pathway
Jianru Shi,Jian Guan,Bingbing Jiang,Daniel A. Brenner,Federica del Monte,Jennifer E. Ward,Lawreen H. Connors,Douglas B. Sawyer,Marc J. Semigran,Thomas E. MacGillivray,David C. Seldin,Rodney H. Falk,Ronglih Liao +12 more
TL;DR: Treatment of cardiomyocytes with SB203580, a selective p38 MAPK inhibitor, significantly attenuated AL-LC–induced oxidative stress, cellular dysfunction, and apoptosis and suggest that TAB1-mediated p38α MAPK autophosphorylation may serve as an important event leading to cardiac dysfunction and subsequent heart failure.
308
Glucose-6-Phosphate Dehydrogenase Modulates Cytosolic Redox Status and Contractile Phenotype in Adult Cardiomyocytes
Mohit Jain,Daniel A. Brenner,Lei Cui,Chee Chew Lim,Bo Wang,David R. Pimentel,Stanley G. Koh,Douglas B. Sawyer,Jane A. Leopold,Diane E. Handy,Joseph Loscalzo,Carl S. Apstein,Ronglih Liao +12 more
TL;DR: It is found that in adult cardiomyocytes, G6PD activity is rapidly increased in response to cellular oxidative stress, with translocation of G6 PD to the cell membrane, and it is concluded that G 6PD is a critical cytosolic antioxidant enzyme, essential for maintenance of cytOSolic redox status in adultCardiomyocyte.
206
Mice Lacking Inducible Nitric Oxide Synthase Have Improved Left Ventricular Contractile Function and Reduced Apoptotic Cell Death Late After Myocardial Infarction
Flora Sam,Douglas B. Sawyer,Zhonglin Xie,Donny L.F. Chang,Soeun Ngoy,Daniel A. Brenner,Deborah A. Siwik,Krishna Singh,Carl S. Apstein,Wilson S. Colucci +9 more
TL;DR: NOS2 does not play an important role in determining infarct size or early LV remodeling during the first month after myocardial infarction, and during late (ie, 4 months after MI) remodeling, NOS2 in remote myocardium contributes to decreased contractile function, increased myocyte apoptosis in remoteMyocardium, and reduced survival.
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