Profiling metabolic remodeling in PP2Acα deficiency and chronic pressure overload mouse hearts

被引：13

作者：

Dong, Dachuan ^{[1
]}

Li, Liangyuan ^{[1
]}

Gu, Pengyu ^{[2
]}

Jin, Tao ^{[1
]}

Wen, Mingda ^{[1
]}

Yuan, Caihua ^{[1
]}

Gao, Xiang ^{[2
]}

Liu, Chang ^{[1
]}

Zhang, Zhao ^{[1
]}

机构：

[1] Nanjing Normal Univ, Coll Life Sci, Jiangsu Key Lab Mol & Med Biotechnol, Nanjing 210023, Jiangsu, Peoples R China

[2] Nanjing Univ, Model Anim Res Ctr, Nanjing 210061, Jiangsu, Peoples R China

来源：

FEBS LETTERS | 2015年 / 589卷 / 23期

基金：

中国国家自然科学基金;

关键词：

Protein phosphatase 2a; Myocardial energetics; Heart failure; Transcriptional profiling; PROTEIN PHOSPHATASE 2A; FATTY-ACID OXIDATION; CORONARY-ARTERY-DISEASE; CATALYTIC SUBUNIT; FAILING HEART; SERINE/THREONINE PHOSPHATASES; FAILURE; DYSFUNCTION; MITOCHONDRIA; HYPERTROPHY;

D O I：

10.1016/j.febslet.2015.10.016

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. PP2Ac alpha 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 PP2Ac alpha 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. (C) 2015 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

引用

页码：3631 / 3639

页数：9

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