Local induction of adiponectin reduces lipopolysaccharide-triggered skeletal muscle damage
Open accessAbstract
Adiponectin (ApN) exhibits metabolic and antiinflammatory properties. This hormone is exclusively secreted by adipocytes under normal conditions. We have shown that ApN was induced in tibialis anterior muscle of mice injected with lipopolysaccharide (LPS) and in C2C12 myotubes cultured with proinflammatory cytokines. We hypothesized that muscle ApN could be a local protective mechanism to counteract excessive inflammatory reaction and oxidative damage. To test this paradigm, we examined whether muscles of ApN-knockout (KO) mice exhibit a higher degree of oxidative stress and apoptosis than wild-type mice when challenged by ip LPS and whether these abnormalities may be corrected by local administration of ApN. Eventually we investigated the effects of ApN in vitro. When compared with wild-type mice, ApN-KO mice exhibited myocyte degenerescence, especially after LPS. Myocytes of ApN-KO mice also displayed much stronger immunolabeling for markers of oxidative stress (peroxiredoxin-3/5 and heme oxygenase-1) as well as for a lipid peroxidation product (hydroxynonenal). Expression of TNF-α, caspase-6, a marker of apoptosis, and nuclear factor-κB was enhanced as well. Eventually muscle electrotransfer of the ApN gene, which did not induce any rise of systemic ApN, corrected all these abnormalities in LPS-injected ApN-KO mice. Likewise, ApN attenuated LPS-induced production of proinflammatory cytokines and activation of nuclear factor-κB in C2C12 cells. Thus, induction of ApN into skeletal muscle in response to an inflammatory aggression appears to be a crucial mechanism to counteract in an autocrine or paracrine fashion excessive inflammatory damage, oxidative stress, and subsequent apoptosis.
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Although mainly secreted by adipocytes under normal conditions, ApN may be produced in skeletal muscle of mice submitted to stressful challenges.
“Although it is mainly secreted by adipocytes under normal conditions, ApN may be produced in skeletal muscle of mice submitted to stressful challenges.”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [40]
Acute (LPS injection) or low-grade inflammation (genetic or nutritional induced obesity) enhanced ApN expression in muscle of challenged mice.
“Thus, acute (lipopolysaccharides (LPS) injection) or low-grade inflammation (genetic or nutritional induced obesity) enhanced ApN expression in muscle of challenged mice [36,38,39,40].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [40]
Muscle electro-transfer of the ApN gene corrected local inflammation, oxidative stress and apoptosis in ApN-KO mice submitted to inflammatory challenge.
“muscle electro-transfer of the ApN gene actually corrected local inflammation, oxidative stress and apoptosis [39,40].”
From Adiponectin and Its Mimics on Skeletal Muscle: Insulin Sensitizers, Fat Burners, Exercise Mimickers, Muscling Pills … or Everything Together? (2020) · cites this paper as [40]
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Self-citation
- Authors
- Jortay, J., Senou, M., Delaigle, A., Noel, L., Funahashi, T., Maeda, N., Many, M. C., & Brichard, S. M.
- Affiliations
- UCLouvain (BE)
- Experimental Morphology Unit (M.S., M.C.M.), Faculty of Medicine, University of Louvain, 1200 Brussels, Belgium
- Endocrinology and Metabolism Unit (J.J., A.D., L.N., S.M.B.), Faculty of Medicine, University of Louvain, 1200 Brussels, Belgium
- The University of Osaka (JP)
- ORCID
- Maeda, Norikazu
- Venue
- Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2010-08-11
- Volume
- 151
- Issue
- 10
- Pages
- 4840-4851
- ISSN
- 0013-7227 (ISSN-L)
- 1945-7170
- OpenAlex
- W2025864341
- Cited by
- 44
- References
- 58
- Citations by year
- 2023: 1 · 2022: 2 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 4 · 2017: 7 · 2016: 6 · 2015: 3 · 2014: 2 · 2013: 3 · 2012: 7
- FWCI
- 1.82
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Licence
- other-oa
- Locations
- Endocrinology (publishedVersion)
- PubMed (publishedVersion)
- DIAL (Catholic University of Leuven) (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- adiponectin, lipopolysaccharide, skeletal muscle injury, muscle inflammation, oxidative stress, apoptosis, adiponectin knockout mice, electrotransfer, inflammatory cytokines, NF-κB, TNF-α, caspase-6, heme oxygenase-1, peroxiredoxin, 4-hydroxynonenal, autocrine and paracrine signaling
- MeSH terms
- Animals, Body Weight, Cells, Cultured, Inflammation, Lipopolysaccharides, Male, Mice, Inbred C57BL, Muscular Diseases, Organ Size, Injections, Intralesional, NF-kappa B, Apoptosis, Mice, Knockout, Oxidative Stress, Muscle, Skeletal, Mice, Adiponectin
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