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Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice

Skeletal muscle repair is initiated by local inflammation and involves the engulfment of dead cells (efferocytosis) by infiltrating macrophages at the injury site. Macrophages orchestrate the whole repair program, and efferocytosis is a key event not only for cell clearance but also for triggering t...

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Autores principales: Tarban, Nastaran, Halász, Hajnalka, Gogolák, Péter, Garabuczi, Éva, Moise, Alexander R., Palczewski, Krzysztof, Sarang, Zsolt, Szondy, Zsuzsa
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9028072/
https://www.ncbi.nlm.nih.gov/pubmed/35456012
http://dx.doi.org/10.3390/cells11081333
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author Tarban, Nastaran
Halász, Hajnalka
Gogolák, Péter
Garabuczi, Éva
Moise, Alexander R.
Palczewski, Krzysztof
Sarang, Zsolt
Szondy, Zsuzsa
author_facet Tarban, Nastaran
Halász, Hajnalka
Gogolák, Péter
Garabuczi, Éva
Moise, Alexander R.
Palczewski, Krzysztof
Sarang, Zsolt
Szondy, Zsuzsa
author_sort Tarban, Nastaran
collection PubMed
description Skeletal muscle repair is initiated by local inflammation and involves the engulfment of dead cells (efferocytosis) by infiltrating macrophages at the injury site. Macrophages orchestrate the whole repair program, and efferocytosis is a key event not only for cell clearance but also for triggering the timed polarization of the inflammatory phenotype of macrophages into the healing one. While pro-inflammatory cytokines produced by the inflammatory macrophages induce satellite cell proliferation and differentiation into myoblasts, healing macrophages initiate the resolution of inflammation, angiogenesis, and extracellular matrix formation and drive myoblast fusion and myotube growth. Therefore, improper efferocytosis results in impaired muscle repair. Retinol saturase (RetSat) initiates the formation of various dihydroretinoids, a group of vitamin A derivatives that regulate transcription by activating retinoid receptors. Previous studies from our laboratory have shown that RetSat-null macrophages produce less milk fat globule-epidermal growth factor-factor-8 (MFG-E8), lack neuropeptide Y expression, and are characterized by impaired efferocytosis. Here, we investigated skeletal muscle repair in the tibialis anterior muscle of RetSat-null mice following cardiotoxin injury. Our data presented here demonstrate that, unexpectedly, several cell types participating in skeletal muscle regeneration compensate for the impaired macrophage functions, resulting in normal muscle repair in the RetSat-null mice.
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spelling pubmed-90280722022-04-23 Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice Tarban, Nastaran Halász, Hajnalka Gogolák, Péter Garabuczi, Éva Moise, Alexander R. Palczewski, Krzysztof Sarang, Zsolt Szondy, Zsuzsa Cells Article Skeletal muscle repair is initiated by local inflammation and involves the engulfment of dead cells (efferocytosis) by infiltrating macrophages at the injury site. Macrophages orchestrate the whole repair program, and efferocytosis is a key event not only for cell clearance but also for triggering the timed polarization of the inflammatory phenotype of macrophages into the healing one. While pro-inflammatory cytokines produced by the inflammatory macrophages induce satellite cell proliferation and differentiation into myoblasts, healing macrophages initiate the resolution of inflammation, angiogenesis, and extracellular matrix formation and drive myoblast fusion and myotube growth. Therefore, improper efferocytosis results in impaired muscle repair. Retinol saturase (RetSat) initiates the formation of various dihydroretinoids, a group of vitamin A derivatives that regulate transcription by activating retinoid receptors. Previous studies from our laboratory have shown that RetSat-null macrophages produce less milk fat globule-epidermal growth factor-factor-8 (MFG-E8), lack neuropeptide Y expression, and are characterized by impaired efferocytosis. Here, we investigated skeletal muscle repair in the tibialis anterior muscle of RetSat-null mice following cardiotoxin injury. Our data presented here demonstrate that, unexpectedly, several cell types participating in skeletal muscle regeneration compensate for the impaired macrophage functions, resulting in normal muscle repair in the RetSat-null mice. MDPI 2022-04-13 /pmc/articles/PMC9028072/ /pubmed/35456012 http://dx.doi.org/10.3390/cells11081333 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Tarban, Nastaran
Halász, Hajnalka
Gogolák, Péter
Garabuczi, Éva
Moise, Alexander R.
Palczewski, Krzysztof
Sarang, Zsolt
Szondy, Zsuzsa
Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
title Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
title_full Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
title_fullStr Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
title_full_unstemmed Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
title_short Regenerating Skeletal Muscle Compensates for the Impaired Macrophage Functions Leading to Normal Muscle Repair in Retinol Saturase Null Mice
title_sort regenerating skeletal muscle compensates for the impaired macrophage functions leading to normal muscle repair in retinol saturase null mice
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9028072/
https://www.ncbi.nlm.nih.gov/pubmed/35456012
http://dx.doi.org/10.3390/cells11081333
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