TY - JOUR
T1 - Recombinant mitochondrial transcription factor A protein inhibits nuclear factor of activated T cells signaling and attenuates pathological hypertrophy of cardiac myocytes
AU - Fujino, Takeo
AU - Ide, Tomomi
AU - Yoshida, Masayoshi
AU - Onitsuka, Ken
AU - Tanaka, Atsushi
AU - Hata, Yuko
AU - Nishida, Motohiro
AU - Takehara, Takako
AU - Kanemaru, Takaaki
AU - Kitajima, Naoyuki
AU - Takazaki, Shinya
AU - Kurose, Hitoshi
AU - Kang, Dongchon
AU - Sunagawa, Kenji
N1 - Funding Information:
This work was supported by Grant-in-Aid for Scientific Research (S) (23220013) and for Scientific Research (C) (23591084) from the Japan Society for the Promotion of Science .
Funding Information:
We thank Ms. Michiyo Tanaka for technical assistant. We appreciate the technical support from the Research Support Center, Graduate School of Medical Sciences, Kyushu University.
Copyright:
Copyright 2013 Elsevier B.V., All rights reserved.
PY - 2012/7
Y1 - 2012/7
N2 - 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.
AB - 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.
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U2 - 10.1016/j.mito.2012.06.002
DO - 10.1016/j.mito.2012.06.002
M3 - Article
C2 - 22709542
AN - SCOPUS:84863731701
SN - 1567-7249
VL - 12
SP - 449
EP - 458
JO - Mitochondrion
JF - Mitochondrion
IS - 4
ER -