Pim1 knockout alleviates sarcopenia in aging mice via reducing adipogenic differentiation of PDGFRα + mesenchymal progenitors
Autor: | Ming Song, Guo-Kai Shang, Wei Zhang, Ming Zhong, Yulin Li, Yi-Hui Li, Lu Han, Zhi-Hao Wang, Yan-Min Tan, Di Wang |
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Rok vydání: | 2021 |
Předmět: |
Aging
Sarcopenia medicine.medical_specialty Adipose tissue Diseases of the musculoskeletal system Basal (phylogenetics) Atrophy Physiology (medical) Internal medicine medicine Orthopedics and Sports Medicine Progenitor cell PDGFRα+ mesenchymal progenitors business.industry QM1-695 Mesenchymal stem cell medicine.disease Pim1 Endocrinology Intramuscular adipose tissue RC925-935 Adipogenesis Adipogenic differentiation Human anatomy PAX7 business |
Zdroj: | Journal of Cachexia, Sarcopenia and Muscle, Vol 12, Iss 6, Pp 1741-1756 (2021) |
ISSN: | 2190-6009 2190-5991 |
DOI: | 10.1002/jcsm.12770 |
Popis: | Background Sarcopenia widely exists in elderly people and triggers numerous age‐related events. The essential pathologic change lies in the increased intramuscular adipose tissue after aging with no exception to non‐obese objects. Pim1 appears to be associated with adipogenic differentiation in recent studies, inspiring us to explore whether it regulates adipogenesis in aging muscles and affects sarcopenia. Methods Wild‐type and Pim1 knockout C57/BL6J mice were randomized into young and old groups. Histo‐pathological and molecular biological methods were applied to assess the intramuscular adipose tissue content, the atrophy and regeneration, and the expressions of Pim1 and adipogenic transcription factors. PDGFRα+ mesenchymal progenitors were separated and their replicative aging model were established. Different time of adipogenic induction and different amounts of Pim1 inhibitor were applied, after which the adipogenic potency were evaluated. The expressions of Pim1 and adipogenic transcription factors were measured through western blotting. Results The aging mice demonstrated decreased forelimb grip strength (P = 0.0003), hanging impulse (P |
Databáze: | OpenAIRE |
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