PMID- 30905858
OWN - NLM
STAT- MEDLINE
DCOM- 20191203
LR  - 20191203
IS  - 1879-3177 (Electronic)
IS  - 0887-2333 (Linking)
VI  - 58
DP  - 2019 Aug
TI  - Rapamycin-induced autophagy decreases Myf5 and MyoD proteins in C2C12 myoblast 
      cells.
PG  - 132-141
LID - S0887-2333(18)30514-9 [pii]
LID - 10.1016/j.tiv.2019.03.025 [doi]
AB  - Rapamycin is an immunosuppressant that inhibits the mammalian or mechanistic 
      target of rapamycin (mTOR) protein kinase and extends lifespan in organisms 
      including mice. Myf5 and MyoD act as muscle-specific transcriptional factors for 
      skeletal muscle differentiation. In this study, we determined whether 
      rapamycin-induced autophagy causes the decrease of Myf5 and MyoD protein in C2C12 
      myoblast cells. Rapamycin induced a significant increase in the expression of the 
      microtubule-associated protein 1 light chain 3 (LC3) II protein in a 
      dose-dependent manner for 12 h. Rapamycin treatment also significantly increased 
      p-ERK, p-Akt, and catalase expressions, and decreased Mn-SOD expression in a 
      dose-dependent manner. Bax expression was significantly high compared to Bcl-2 
      expression in a dose-dependent manner of rapamycin for 12 h. For further study of 
      rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin 
      treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin 
      treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and 
      Bcl-2 proteins were significantly increased compared to without rapamycin. p-ERK 
      expression increased with rapamycin treatment for 24 and 36 h compared to that 
      without rapamycin, but decreased for 48 h. p-Akt expression decreased with 
      rapamycin treatment for 36 and 48 h compared to that without rapamycin. In the 
      same conditions, rapamycin-induced autophagy significantly reduced the Myf5 and 
      MyoD proteins. Together, these results suggest that rapamycin-induced autophagy 
      results in the decrease of Myf5 and MyoD proteins in C2C12 myoblast cells.
CI  - Copyright (c) 2019 Elsevier Ltd. All rights reserved.
FAU - Yoo, Yeong-Min
AU  - Yoo YM
AD  - Laboratory of Veterinary Biochemistry and Molecular Biology, College of 
      Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, 
      Republic of Korea.
FAU - Jung, Eui-Man
AU  - Jung EM
AD  - Laboratory of Veterinary Biochemistry and Molecular Biology, College of 
      Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, 
      Republic of Korea.
FAU - Jeung, Eui-Bae
AU  - Jeung EB
AD  - Laboratory of Veterinary Biochemistry and Molecular Biology, College of 
      Veterinary Medicine, Chungbuk National University, Cheongju, Chungbuk 28644, 
      Republic of Korea. Electronic address: ebjeung@chungbuk.ac.kr.
LA  - eng
PT  - Journal Article
DEP - 20190321
PL  - England
TA  - Toxicol In Vitro
JT  - Toxicology in vitro : an international journal published in association with 
      BIBRA
JID - 8712158
RN  - 0 (Immunosuppressive Agents)
RN  - 0 (Myf5 protein, mouse)
RN  - 0 (MyoD Protein)
RN  - 0 (MyoD1 myogenic differentiation protein)
RN  - 0 (Myogenic Regulatory Factor 5)
RN  - W36ZG6FT64 (Sirolimus)
SB  - IM
MH  - Animals
MH  - Autophagy/*drug effects
MH  - Cell Line
MH  - Immunosuppressive Agents/*toxicity
MH  - Mice
MH  - MyoD Protein/*metabolism
MH  - Myoblasts/*drug effects/metabolism
MH  - Myogenic Regulatory Factor 5/*metabolism
MH  - Sirolimus/*toxicity
OTO - NOTNLM
OT  - Autophagy
OT  - C2C12 myoblast cells
OT  - Myf5
OT  - MyoD
OT  - Rapamycin
EDAT- 2019/03/25 06:00
MHDA- 2019/12/04 06:00
CRDT- 2019/03/26 06:00
PHST- 2018/08/30 00:00 [received]
PHST- 2019/03/20 00:00 [revised]
PHST- 2019/03/20 00:00 [accepted]
PHST- 2019/03/25 06:00 [pubmed]
PHST- 2019/12/04 06:00 [medline]
PHST- 2019/03/26 06:00 [entrez]
AID - S0887-2333(18)30514-9 [pii]
AID - 10.1016/j.tiv.2019.03.025 [doi]
PST - ppublish
SO  - Toxicol In Vitro. 2019 Aug;58:132-141. doi: 10.1016/j.tiv.2019.03.025. Epub 2019 
      Mar 21.