分析PP2Acα缺乏和慢性压力超负荷小鼠心脏中的代谢重塑。
Profiling metabolic remodeling in PP2Acα deficiency and chronic pressure overload mouse hearts.
作者信息
Dong Dachuan, Li Liangyuan, Gu Pengyu, Jin Tao, Wen Mingda, Yuan Caihua, Gao Xiang, Liu Chang, Zhang Zhao
机构信息
Jiangsu Key Laboratory for Molecular and Medical Biotechnology, College of Life Science, Nanjing Normal University, Nanjing 210023, China.
Model Animal Research Center of Nanjing University, Nanjing 210061, China.
出版信息
FEBS Lett. 2015 Nov 30;589(23):3631-9. doi: 10.1016/j.febslet.2015.10.016. Epub 2015 Oct 21.
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.
我们对衰竭心脏中代谢转换如何发生的理解仍然有限。在此，我们报告了两种不同小鼠模型中代谢变化的典型模式。PP2Acα缺陷型心脏中，参与葡萄糖利用的转运蛋白和酶的编码mRNA水平显著降低，这通过控制脂肪酸利用的基因更高的表达水平得到补偿。这些特征在培养的PP2Acα基因敲除心肌细胞中部分重现。同样，在TAC模型中也观察到控制葡萄糖和脂肪酸代谢的大多数转运蛋白和酶的表达下降。
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