Macrophages and skeletal muscle regeneration: a clodronate-containing liposome depletion study
Abstract
The study evaluates the influence of monocytes/macrophages in the mechanisms of skeletal muscle injury using a mouse model and selective depletion of peripheral monocyte with systemic injections of liposomal clodronate (dichloromethylene bisphosphonate). This pharmacological treatment has been demonstrated to induce specific apoptotic death in monocytes and phagocytic macrophages. In the current studies, the liposomal clodronate injections resulted in a marked attenuation of the peak inflammatory response in the freeze-injured muscle in the first three days after injury. The effect was accompanied by a transient reduction (at day 1 or 3 postinjury) of the expression of several genes coding for inflammatory, as well as growth-related mediators, including TNF, monocyte chemoattractant protein (MCP)-1, thioredoxin, high-mobility group AT-hook 1, insulin-like growth factor-binding protein (IGFBP), and IGF-1. In contrast, the expression of major myogenic factors (i.e., MyoD and myogenin) directly involved in the activation/proliferation and differentiation of muscle precursor cells was not altered by the clodronate liposome treatment. The repair process in the injured muscle of clodronate liposome-treated mice was characterized by prolonged clearance of necrotic myofibers and a tendency for increased muscle fat accumulation at day 9 and 14 postinjury, respectively. In conclusion, a significant reduction of the initial monocyte/macrophage influx into the injured muscle is associate…
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Depletion of circulating monocytes reduces removal of cellular debris and delays muscle tissue remodeling after injury.
“A number of studies have shown that reduction of the number of monocytes available to participate in the response following muscle injury via depletion of circulating cells results in slowed removal of cellular debris and delayed muscle tissue remodeling [112–114].”
From Macrophage polarization: an opportunity for improved outcomes in biomaterials and regenerative medicine (2012) · cites this paper as [113]
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Nonmyogenic Cells in Skeletal Muscle Regeneration
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- Authors
- Summan, M., Warren, G. L., Mercer, R. R., Chapman, R., Hulderman, T., Van Rooijen, N., & Simeonova, P. P.
- Affiliations
- National Institute for Occupational Safety and Health (US)
- Centers for Disease Control and Prevention (US)
- Venue
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology
- Publisher
- American Physiological Society
- Published
- 2006-06
- Volume
- 290
- Issue
- 6
- Pages
- R1488-R1495
- ISSN
- 0363-6119 (ISSN-L)
- 1522-1490
- OpenAlex
- W2115825738
- Cited by
- 285
- References
- 2
- Citations by year
- 2026: 6 · 2025: 7 · 2024: 16 · 2023: 9 · 2022: 15 · 2021: 24 · 2020: 21 · 2019: 11 · 2018: 16 · 2017: 19 · 2016: 18 · 2015: 23 · 2014: 12 · 2013: 18 · 2012: 16
- FWCI
- 4.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- American Journal of Physiology-Regulatory, Integrative and Comparative Physiology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Muscle Physiology and Disorders
- Health Sciences › Medicine › Rehabilitation › Wound Healing and Treatments
- Health Sciences › Medicine › Rehabilitation › Exercise and Physiological Responses
- Keywords
- macrophages, skeletal muscle regeneration, clodronate liposomes, frost damage, muscle inflammation, TNF-α, MCP-1, thioredoxin, insulin-like growth factor I, MyoD, myogenin, muscle precursor cells
- MeSH terms
- Animals, Antigens, Differentiation, Cell Nucleus, Clodronic Acid, Female, Immunohistochemistry, Insulin-Like Growth Factor I, Liposomes, Macrophages, Mice, Inbred C57BL, Monocytes, Regeneration, Tumor Necrosis Factor-alpha, Gene Expression, Macrophage-1 Antigen, MyoD Protein, Myogenin, Muscle, Skeletal, Chemokine CCL2, Insulin-Like Growth Factor Binding Proteins, Receptors, Chemokine, Reverse Transcriptase Polymerase Chain Reaction, Mice
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