TY - JOUR
T1 - Bach1 promotes muscle regeneration through repressing Smad-mediated inhibition of myoblast differentiation
AU - Suzuki, Katsushi
AU - Matsumoto, Mitsuyo
AU - Katoh, Yasutake
AU - Liu, Liang
AU - Ochiai, Kyoko
AU - Aizawa, Yuta
AU - Nagatomi, Ryoichi
AU - Okuno, Hiroshi
AU - Itoi, Eiji
AU - Igarashi, Kazuhiko
N1 - Funding Information:
This study was supported by Grants-in-Aid from the Japan Society for the Promotion of Science (18H04021 and 15H02506 to K.I., 19K07680 and 16K07108 to M.M., and 17K10918 to H.O.) We thank T. Kundu, A. Bose, A. Fukamizu and W. Z. Lu for generous help andadvices on C2C12 cells. We are deeply grateful to members of Department of Biochemistry and Department of Orthopaedic Surgery, Tohoku University Graduate School of Medicine, for giving insightful comments and suggestions. We thank Biomedical Research Core of Tohoku University Graduate School of Medicine for use of facilities.
Publisher Copyright:
© 2020 Suzuki et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2020/8
Y1 - 2020/8
N2 - It has been reported that Bach1-deficient mice show reduced tissue injuries in diverse disease models due to increased expression of heme oxygenase-1 (HO-1)that possesses an antioxidant function. In contrast, we found that Bach1 deficiency in mice exacerbated skeletal muscle injury induced by cardiotoxin. Inhibition of Bach1 expression in C2C12 myoblast cells using RNA interference resulted in reduced proliferation, myotube formation, and myogenin expression compared with control cells. While the expression of HO-1 was increased by Bach1 silencing in C2C12 cells, the reduced myotube formation was not rescued by HO-1 inhibition. Up-regulations of Smad2, Smad3 and FoxO1, known inhibitors of muscle cell differentiation, were observed in Bach1-deficient mice and Bach1-silenced C2C12 cells. Therefore, Bach1 may promote regeneration of muscle by increasing proliferation and differentiation of myoblasts.
AB - It has been reported that Bach1-deficient mice show reduced tissue injuries in diverse disease models due to increased expression of heme oxygenase-1 (HO-1)that possesses an antioxidant function. In contrast, we found that Bach1 deficiency in mice exacerbated skeletal muscle injury induced by cardiotoxin. Inhibition of Bach1 expression in C2C12 myoblast cells using RNA interference resulted in reduced proliferation, myotube formation, and myogenin expression compared with control cells. While the expression of HO-1 was increased by Bach1 silencing in C2C12 cells, the reduced myotube formation was not rescued by HO-1 inhibition. Up-regulations of Smad2, Smad3 and FoxO1, known inhibitors of muscle cell differentiation, were observed in Bach1-deficient mice and Bach1-silenced C2C12 cells. Therefore, Bach1 may promote regeneration of muscle by increasing proliferation and differentiation of myoblasts.
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U2 - 10.1371/journal.pone.0236781
DO - 10.1371/journal.pone.0236781
M3 - Article
C2 - 32776961
AN - SCOPUS:85089324586
SN - 1932-6203
VL - 15
JO - PLoS One
JF - PLoS One
IS - 8 August
M1 - e0236781
ER -