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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

MAMMALIAN TARGET OF RAPAMYCIN COMPLEX 1 IS INVOLVED IN DIFFERENTIATION OF REGENERATING MYOFIBERS IN VIVO

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Miyabara, Elen H. [1] ; Conte, Talita C. [1] ; Silva, Meiricris T. [1] ; Baptista, Igor L. [2] ; Bueno, Jr., Carlos [3] ; Fiamoncini, Jarlei [4] ; Lambertucci, Rafael H. [4] ; Serra, Carmen S. [5] ; Brum, Patricia C. [3] ; Pithon-curi, Tania [4] ; Curi, Rui [4] ; Aoki, Marcelo S. [6] ; Oliveira, Antonio C. [5] ; Moriscot, Anselmo S. [2]
Total Authors: 14
Affiliation:
[1] Univ Sao Paulo, Inst Biomed Sci, Dept Anat, BR-05508000 Sao Paulo - Brazil
[2] Univ Sao Paulo, Dept Cell & Dev Biol, BR-05508000 Sao Paulo - Brazil
[3] Univ Sao Paulo, Sch Phys Educ & Sport, Dept Biodynam, BR-05508000 Sao Paulo - Brazil
[4] Univ Sao Paulo, Dept Physiol & Biophys, BR-05508000 Sao Paulo - Brazil
[5] Univ Sao Paulo, Inst Biomed Sci, Dept Pharmacol, BR-05508000 Sao Paulo - Brazil
[6] Univ Sao Paulo, Sch Arts Sci & Humanities, BR-05508000 Sao Paulo - Brazil
Total Affiliations: 6
Document type: Journal article
Source: MUSCLE & NERVE; v. 42, n. 5, p. 778-787, NOV 2010.
Web of Science Citations: 21
Abstract

This work was undertaken to provide further insight into the role of mammalian target of rapamycin complex 1 (mTORC1) in skeletal muscle regeneration, focusing on myofiber size recovery. Rats were treated or not with rapamycin, an mTORC1 inhibitor. Soleus muscles were then subjected to cryolesion and analyzed 1, 10, and 21 days later. A decrease in soleus myofiber cross-section area on post-cryolesion days 10 and 21 was accentuated by rapamycin, which was also effective in reducing protein synthesis in these freeze-injured muscles. The incidence of proliferating satellite cells during regeneration was unaltered by rapamycin, although immunolabeling for neonatal myosin heavy chain (MHC) was weaker in cryolesion+rapamycin muscles than in cryolesion-only muscles. In addition, the decline in tetanic contraction of freeze-injured muscles was accentuated by rapamycin. This study indicates that mTORC1 plays a key role in the recovery of muscle mass and the differentiation of regenerating myofibers, independently of necrosis and satellite cell proliferation mechanisms. Muscle Nerve 42: 778-787,2010 (AU)