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Effects of IL‐6 receptor inhibition and/or heat treatment on the regeneration of injured mouse skeletal muscle
Author(s) -
Fujita Ryo,
Ohira Takashi,
Kami Katsuya,
Oke Yoshihiko,
Nomura Sachiko,
Kawano Fuminori,
Nakai Naoya,
Ohira Yoshinobu
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.989.10
Subject(s) - skeletal muscle , cardiotoxin , myogenin , desmin , regeneration (biology) , medicine , immunohistochemistry , endocrinology , chemistry , myogenesis , biology , microbiology and biotechnology , vimentin
Effects of inhibited interleukin‐6 (IL‐6) signal using the rat anti‐mouse IL6 receptor (MR16‐1) with or without heat treatment on the regeneration of injured skeletal muscle was studied in mice. 10‐week‐old C57BL/6JJc1 mice were divided into 5 groups: (1) normal controls, (2) cardiotoxin injection (CTX), (3) administration of MR16‐1 after CTX injection (CTX‐MR), (4) heat treatment after CTX injection (CTX‐H), and (5) administration of MR16‐1 plus heat treatment after CTX injection (CTX‐MR‐H). The CTX (10 μl) was injected into the right tibialis anterior (TA) muscle. MR16‐1 (2 mg) was injected i.p immediately after CTX injection. For heat treatment, the conscious mice were placed in a heat chamber (42 °C) for 60 min 1, 3, and 5 days after CTX injection. Muscles were sampled 7 days after these treatments and cross‐sectional analyses were performed. Regenerating myofibers with centrally located nuclei were noted 7 days after CTX injection. Immunohistochemical analyses revealed that desmin‐ and dystrophin‐positive (+) cells were increased in CTX‐MR and CTX‐MR‐H groups. Further, a number of myogenin + cells were seen in the damaged myofibers of CTX‐H group. These results suggest that blockage of IL‐6 signal and heat treatment facilitate the regeneration of skeletal muscle. This study was supported by Grant‐in‐Aid for Scientific Research S (19100009) from the Japan Society for the Promotion of Science.