Recombinant mitochondrial transcription factor A protein inhibits nuclear factor of activated T cells signaling and attenuates pathological hypertrophy of cardiac myocytes
Recombinant mitochondrial transcription factor A protein inhibits nuclear factor of activated T cells signaling and attenuates pathological hypertrophy of cardiac myocytes
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DOI：
10.1016/j.mito.2012.06.002
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发表时间：
2012-07-01
期刊：
影响因子：
4.4
通讯作者：
Sunagawa, Kenji
中科院分区：
文献类型：
--
作者：
Fujino, Takeo;Ide, Tomomi;Sunagawa, Kenji
线粒体转录因子A（TFAM）的过度表达可减轻心肌梗死后线粒体DNA拷贝数的减少，改善病理性肥大，并显著提高生存率。然而，非转基因策略，以增加线粒体DNA的治疗病理性肥大仍然未知。我们生产了重组人TFAM蛋白（rhTFAM）。rhTFAM能迅速进入培养心肌细胞线粒体。rhTFAM增加mtDNA并消除活化T细胞核因子（NFAT）的活化，这是众所周知的激活病理性肥大。rhTFAM也减弱了随后的肌细胞形态学肥大。rhTFAM可能是一种有吸引力的减轻心肌病理性肥大的分子。(C)2012 Elsevier B.V.和线粒体研究学会。All rights reserved.
The overexpression of mitochondrial transcription factor A (TFAM) attenuates the decrease in mtDNA copy number after myocardial infarction, ameliorates pathological hypertrophy, and markedly improves survival. However, non-transgenic strategy to increase mtDNA for the treatment of pathological hypertrophy remains unknown. We produced recombinant human TFAM protein (rhTFAM). rhTFAM rapidly entered into mitochondria of cultured cardiac myocytes. rhTFAM increased mtDNA and abolished the activation of nuclear factor of activated T cells (NFAT), which is well known to activate pathological hypertrophy. rhTFAM attenuated subsequent morphological hypertrophy of myocytes as well. rhTFAM would be an attractive molecule in attenuating cardiac pathological hypertrophy. (C) 2012 Elsevier B.V. and Mitochondria Research Society. All rights reserved.