In situ macrophage phenotypic transition is affected by altered cellular composition prior to acute sterile muscle injury Article Swipe
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· 2017
· Open Access
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· DOI: https://doi.org/10.1113/jp274361
Key points The in situ phenotypic switch of macrophages is delayed in acute injury following irradiation. The combination of bone marrow transplantation and local muscle radiation protection allows for the identification of a myeloid cell contribution to tissue repair. PET‐MRI allows monitoring of myeloid cell invasion and metabolism. Altered cellular composition prior to acute sterile injury affects the in situ phenotypic transition of invading myeloid cells to repair macrophages. There is reciprocal intercellular communication between local muscle cell compartments, such as PAX7 positive cells, and recruited macrophages during skeletal muscle regeneration. Abstract Skeletal muscle regeneration is a complex interplay between various cell types including invading macrophages. Their recruitment to damaged tissues upon acute sterile injuries is necessary for clearance of necrotic debris and for coordination of tissue regeneration. This highly dynamic process is characterized by an in situ transition of infiltrating monocytes from an inflammatory (Ly6C high ) to a repair (Ly6C low ) macrophage phenotype. The importance of the macrophage phenotypic shift and the cross‐talk of the local muscle tissue with the infiltrating macrophages during tissue regeneration upon injury are not fully understood and their study lacks adequate methodology. Here, using an acute sterile skeletal muscle injury model combined with irradiation, bone marrow transplantation and in vivo imaging, we show that preserved muscle integrity and cell composition prior to the injury is necessary for the repair macrophage phenotypic transition and subsequently for proper and complete tissue regeneration. Importantly, by using a model of in vivo ablation of PAX7 positive cells, we show that this radiosensitive skeletal muscle progenitor pool contributes to macrophage phenotypic transition following acute sterile muscle injury. In addition, local muscle tissue radioprotection by lead shielding during irradiation preserves normal macrophage transition dynamics and subsequently muscle tissue regeneration. Taken together, our data suggest the existence of a more extensive and reciprocal cross‐talk between muscle tissue compartments, including satellite cells, and infiltrating myeloid cells upon tissue damage. These interactions shape the macrophage in situ phenotypic shift, which is indispensable for normal muscle tissue repair dynamics. image
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- Type
- article
- Language
- en
- Landing Page
- https://doi.org/10.1113/jp274361
- OA Status
- green
- Cited By
- 48
- References
- 92
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2735908238
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2735908238Canonical identifier for this work in OpenAlex
- DOI
-
https://doi.org/10.1113/jp274361Digital Object Identifier
- Title
-
In situ macrophage phenotypic transition is affected by altered cellular composition prior to acute sterile muscle injuryWork title
- Type
-
articleOpenAlex work type
- Language
-
enPrimary language
- Publication year
-
2017Year of publication
- Publication date
-
2017-07-17Full publication date if available
- Authors
-
Andreas Patsalos, Attila Pap, Tamás Varga, György Trencsényi, Gerardo Alvarado Contreras, Ildiko Garai, Z. Papp, Balázs Dezső, Éva Pintye, László NagyList of authors in order
- Landing page
-
https://doi.org/10.1113/jp274361Publisher landing page
- Open access
-
YesWhether a free full text is available
- OA status
-
greenOpen access status per OpenAlex
- OA URL
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https://hdl.handle.net/2437/243079Direct OA link when available
- Concepts
-
Regeneration (biology), Macrophage, Skeletal muscle, Cell biology, Biology, Pathology, Transplantation, Bone marrow, Phenotype, In vivo, Immunology, Medicine, Anatomy, In vitro, Internal medicine, Biochemistry, Genetics, GeneTop concepts (fields/topics) attached by OpenAlex
- Cited by
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48Total citation count in OpenAlex
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2025: 7, 2024: 4, 2023: 5, 2022: 5, 2021: 7Per-year citation counts (last 5 years)
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92Number of works referenced by this work
- Related works (count)
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10Other works algorithmically related by OpenAlex
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