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Koike, T. E.

Publications and source records attributed to Koike, T. E..

2 recordsLinked to original sources

The IRE1α/XBP1/Myomaker axis drives myoblast fusion in adult skeletal muscle

Skeletal muscle regeneration involves a signaling network that regulates the proliferation, differentiation, and fusion of muscle precursor cells to injured myofibers. Inositol requiring enzyme 1 alpha (IRE1) is one of the arms of the unfolded protein response (UPR) that regulates cellular proteostasis in response to ER stress. Here, we demonstrate that inducible deletion of IRE1 in adult muscle stem cells (i.e. satellite cells) of mice impairs skeletal muscle regeneration primarily through inhibiting myoblast fusion step. Knockdown of IRE1 or its downstream target, X-box protein 1 (XBP1), also inhibits fusion of cultured myoblasts during myogenesis. Genome-wide transcriptome analysis revealed that knockdown of IRE1 or XBP1 deregulates the gene expression of molecules involved in the regulation of myoblast fusion. The IRE1-XBP1 axis mediates the gene expression of multiple profusion molecules, including Myomaker (Mymk) during myogenic differentiation. Our study demonstrates that spliced XBP1 (sXBP1) transcription factor binds to the promoter region of Mymk gene during myogenesis. Overexpression of myomaker in IRE1-knockdown cultures rescues fusion defects. Finally, our results show that inducible deletion of IRE1 in satellite cells inhibits myoblast fusion and myofiber hypertrophy in response to functional overload. Collectively, our study demonstrates that IRE1 promotes myoblast fusion through sXBP1-mediated up-regulation in the gene expression of profusion molecules. Significance StatementMyoblast fusion is an essential step for regeneration and post-natal growth of skeletal muscle. We demonstrate that the activation of the IRE1/XBP1 arm of the unfolded protein response induces myoblast fusion through augmenting the gene expression of multiple profusion molecules, including myomaker. This study has identified a novel signaling axis that link ER stress-induced non-myogenic signaling pathway to myoblast fusion. Augmenting the activity of IRE1/XBP1 pathway could be a potential therapeutic strategy for various muscle degenerative diseases.

cell biology↗

Temporal regulation of TAK1 to counteract muscular dystrophy

Muscular dystrophy is a group of genetic neuromuscular disorders that involves severe muscle wasting. Transforming growth factor {beta}-activated kinase 1 (TAK1) is an important signaling protein that regulates cell survival, growth, and inflammation. TAK1 has been recently found to promote myofiber growth in skeletal muscle of adult mice. However, the role of TAK1 in muscle disorders remains poorly understood. In the present study, we have investigated how TAK1 affects progression of dystrophic phenotype in the mdx mouse model of Duchnne muscular dystrophy (DMD). TAK1 is highly activated during peak necrotic phase in mdx mice. Targeted inducible inactivation of TAK1 inhibits muscle injury, necroptosis, and accumulation of macrophages in dystrophic muscle of mdx mice. Additionally, targeted inactivation of TAK1 leads to the activation of autophagy and Notch and Wnt signaling in the dystrophic muscle. However, inactivation of TAK1 significantly reduces myofiber size and muscle contractile function in both young and adult mdx mice. Forced activation of TAK1 in skeletal muscle after peak necrotic phase induces myofiber growth and improves muscle histopathology in mdx mice. Our results suggest that targeted activation of TAK1 can ameliorate disease progression and improve muscle growth in DMD. One Sentence SummaryOur results demonstrate that duly regulation of TAK1 activity ameliorates dystrophic phenotype in a mouse model of Duchnne Muscular Dystrophy.

physiology↗