Adiponectin promotes muscle regeneration through binding to T-cadherin
Open accessAbstract
Skeletal muscle has remarkable regenerative potential and its decline with aging is suggested to be one of the important causes of loss of muscle mass and quality of life in elderly adults. Metabolic abnormalities such as obesity were linked with decline of muscle regeneration. On the other hand, plasma levels of adiponectin are decreased in such metabolic conditions. However, plasma levels of adiponectin have been shown to inversely correlate with muscle mass and strength in elderly people especially with chronic heart failure (CHF). Here we have addressed whether adiponectin has some impact on muscle regeneration after cardiotoxin-induced muscle injury in mice. Muscle regeneration was delayed by angiotensin II infusion, mimicking aging and CHF as reported. Adiponectin overexpression in vivo decreased necrotic region and increased regenerating myofibers. Such enhanced regeneration by excess adiponectin was also observed in adiponectin null mice, but not in T-cadherin null mice. Mechanistically, adiponectin accumulated on plasma membrane of myofibers both in mice and human, and intracellularly colocalized with endosomes positive for a multivesicular bodies/exosomes marker CD63 in regenerating myofibers. Purified high-molecular multimeric adiponectin similarly accumulated intracellularly and colocalized with CD63-positive endosomes and enhanced exosome secretion in differentiating C2C12 myotubes but not in undifferentiated myoblasts. Knockdown of T-cadherin in differentiating C2C12 myotubes attenuated both adiponectin-accumulation and adiponectin-mediated exosome production. Collectively, our studies have firstly demonstrated that adiponectin stimulates muscle regeneration through T-cadherin, where intracellular accumulation and exosome-mediated process of adiponectin may have some roles.
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T-cadherin mediates skeletal muscle regeneration by HMW ApN.
“This receptor further mediates cardiovascular protection [14,15] and skeletal muscle regeneration by HMW ApN [16].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [16]
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- Authors
- Tanaka, Y., Kita, S., Nishizawa, H., Fukuda, S., Fujishima, Y., Obata, Y., Nagao, H., Masuda, S., Nakamura, Y., Shimizu, Y., Mineo, R., Natsukawa, T., Funahashi, T., Ranscht, B., Fukada, S.-I., Maeda, N., & Shimomura, I.
- Affiliations
- The University of Osaka (JP)
- Yodogawa Christian Hospital (JP)
- Sanford Burnham Prebys Medical Discovery Institute (US)
- Corresponding author
- Kita, Shunbun
- ORCID
- Venue
- Scientific Reports
- Published
- 2019-01-09
- Volume
- 9
- Issue
- 1
- Pages
- 16-16
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6327035
- OpenAlex
- W2910728038
- Cited by
- 103
- References
- 47
- Citations by year
- 2026: 14 · 2025: 14 · 2024: 13 · 2023: 12 · 2022: 11 · 2021: 18 · 2020: 15 · 2019: 6
- FWCI
- 4.14
- Type
- journal article
- Language
- en
- Update notices
- correction (2020-07-17)
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Japan Foundation for Applied Enzymology
- Japan Society for the Promotion of Science (16K09801, 18H02863, 16K09802, 15H04853)
- Core Research for Evolutional Science and Technology
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- adiponectin, T-cadherin, skeletal muscle regeneration, cardiotoxin-induced muscle injury, exosomes, CD63, endosomes, angiotensin II, chronic heart failure, muscle aging, obesity, myofiber regeneration, C2C12 myotubes
- MeSH terms
- Aging, Animals, Cell Line, Heart Failure, Humans, Mice, Inbred C57BL, Regeneration, Cadherins, Muscle, Skeletal, Mice, Adiponectin
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