Suppression of MyoD induces spontaneous adipogenesis in skeletal muscle progenitor cell culture
Autor: | Shiho Takeuchi, Takashi Matsuwaki, Tohru Hosoyama, Masugi Nishihara, Katsuyuki Nakamura, Keitaro Yamanouchi |
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Rok vydání: | 2021 |
Předmět: |
Adipogenesis
Satellite Cells Skeletal Muscle Myogenesis Chemistry Stem Cells Mesenchymal stem cell Muscle Fibers Skeletal Adipose tissue Skeletal muscle General Medicine medicine.disease MyoD Cell biology Rats medicine.anatomical_structure medicine Animals Muscular dystrophy Progenitor cell General Agricultural and Biological Sciences Muscle Skeletal |
Zdroj: | Animal science journal = Nihon chikusan GakkaihoREFERENCES. 92(1) |
ISSN: | 1740-0929 |
Popis: | The degree of intramuscular adipose tissue accumulation is one of the factors affecting meat quality. Accumulation of adipocytes is also observed under the pathological condition of skeletal muscle such as muscular dystrophy and sarcopenia. The origin of adipocytes seen in skeletal muscle is mesenchymal progenitor cells that can give rise to both adipocytes and fibroblasts. In the present study, we demonstrated that siRNA-mediated suppression of MyoD expression in rat skeletal muscle progenitor cell culture, which comprises both myogenic satellite cells and mesenchymal progenitor cells, resulted in diminished myotube formation and an unexpected spontaneous appearance of white adipocytes. Suppressing myomaker expression also resulted in complete absence of myotube formation without reducing MyoD expression, but no adipogenesis was seen in this scenario, indicating that decline in MyoD expression rather than decreased myotube formation is necessary to induce adipogenesis. In addition, spontaneous adipogenesis induced by suppressing MyoD expression in culture was inhibited by the conditioned medium from control culture, indicating that anti-adipogenic factor(s) are secreted from MyoD-positive myogenic cells. These results indicate the presence of regulatory mechanism on adipogenesis by myogenic cells. |
Databáze: | OpenAIRE |
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