Open AccessTLR4‐defective (C3H/HeJ) mice are not protected from cast immobilization‐induced muscle atrophy
Author(s) -
Kawanishi Noriaki,
Nozaki Risa,
Naito Hisashi,
Machida Shuichi
Publication year - 2017
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.13255
Subject(s) - muscle atrophy , tlr4 , atrophy , gastrocnemius muscle , medicine , endocrinology , inflammation , chemistry , skeletal muscle , proinflammatory cytokine
Recent studies have shown that activation of Toll‐like receptor ( TLR )4 signaling may be an important factor in muscle atrophy and excessive inflammatory response associated with immobilization. To examine the role of TLR 4 signaling on cast immobilization‐induced skeletal muscle atrophy, we tested the hypothesis that muscle atrophy and inflammation after cast immobilization is reduced in TLR 4‐defective mice. TLR 4‐defective (C3H/HeJ) and wild type (C3H/HeN) mice were divided into control and cast‐immobilization groups. Cast immobilization was imposed for 14 days. Cast immobilization increased TLR4 mRNA expression in the gastrocnemius and decreased muscle mass and cross‐sectional area ( CSA ) of the gastrocnemius fibers. However, there was no difference in the gastrocnemius muscle mass and CSA between TLR 4‐defective and wild type mice. Cast immobilization‐induced increase in ubiquitin E3 ligases (MAFbx/Atrogin‐1 and MuRF1), inflammatory cytokines, and macrophage/monocyte marker mRNA s were unaffected by defective TLR 4. Our findings in C3H/HeJ mice suggested that TLR 4 signaling might not play an essential role in immobilization‐induced muscle atrophy.