Profiling metabolic remodeling in PP2Acα deficiency and chronic pressure overload mouse hearts.
Our understanding of how metabolic switches occur in the failing heart is still limited. Here, we report the emblematic pattern of metabolic alternations in two different mouse models. PP2Acα deficient hearts exhibited a dramatic decrease in the levels of mRNA encoding for transporters and enzymes involved in glucose utilization, which compensated by higher expression levels of genes controlling fatty acid utilization. These features were partly reproduced in cultured PP2Acα KD cardiomyocytes. Equivalently, a decrease in the expression of most of the transporters and enzymes controlling both glucose and fatty acid metabolism were observed in TAC model.
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Dachuan
D
Dong
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Liangyuan
L
Li
Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Pengyu
P
Gu
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Tao
T
Jin
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Mingda
M
Wen
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Caihua
C
Yuan
Model Animal Research Center of Nanjing University, Nanjing 210061, China.
Xiang
X
Gao
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Chang
C
Liu
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China. Electronic address: zhangzhao@njnu.edu.cn.
Zhao
Z
Zhang
D000222:Adaptation, Physiological; D000818:Animals; D009202:Cardiomyopathies / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology*; D006984:Hypertrophy / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D009928:Organ Specificity; D011312:Pressure / Q000009:adverse effects*; D054648:Protein Phosphatase 2 / Q000172:deficiency*; D013312:Stress, Physiological; D013997:Time Factors
C578496:PPP2CA protein, mouse; D054648:Protein Phosphatase 2
Heart failure; Myocardial energetics; Protein phosphatase 2a; Transcriptional profiling