Identification of Periostin as a critical niche for myofibroblast dynamics and fibrosis during tendon healing.

Autor:	Ackerman JE; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Current affiliation: NDORMS, University of Oxford, Oxford, United Kingdom., Adjei-Sowah E; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Department of Biomedical Engineering, University of Rochester, Rochester, NY., Korcari A; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Department of Biomedical Engineering, University of Rochester, Rochester, NY., Muscat SN; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Department of Pathology & Laboratory Medicine, University of Rochester Medical Center, Rochester, NY., Nichols AEC; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Department of Orthopaedics & Physical Performance, University of Rochester Medical Center, Rochester, NY., Buckley MR; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Department of Biomedical Engineering, University of Rochester, Rochester, NY., Loiselle AE; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, NY.; Department of Biomedical Engineering, University of Rochester, Rochester, NY.; Department of Pathology & Laboratory Medicine, University of Rochester Medical Center, Rochester, NY.; Department of Orthopaedics & Physical Performance, University of Rochester Medical Center, Rochester, NY.
Jazyk:	angličtina
Zdroj:	BioRxiv : the preprint server for biology [bioRxiv] 2023 Jul 21. Date of Electronic Publication: 2023 Jul 21.
DOI:	10.1101/2023.07.21.550090
Abstrakt:	Tendon injuries are a major clinical problem, with poor patient outcomes caused by abundant scar tissue deposition during healing. Myofibroblasts play a critical role in the initial restoration of structural integrity after injury. However, persistent myofibroblast activity drives the transition to fibrotic scar tissue formation. As such, disrupting myofibroblast persistence is a key therapeutic target. While myofibroblasts are typically defined by the presence of αSMA+ stress fibers, αSMA is expressed in other cell types including the vasculature. As such, modulation of myofibroblast dynamics via disruption of αSMA expression is not a translationally tenable approach. Recent work has demonstrated that Periostin-lineage (Postn Lin ) cells are a precursor for cardiac fibrosis-associated myofibroblasts. In contrast to this, here we show that Postn Lin cells contribute to a transient αSMA+ myofibroblast population that is required for functional tendon healing, and that Periostin forms a supportive matrix niche that facilitates myofibroblast differentiation and persistence. Collectively, these data identify the Periostin matrix niche as a critical regulator of myofibroblast fate and persistence that could be targeted for therapeutic manipulation to facilitate regenerative tendon healing. Competing Interests: Competing interests: The authors declare that there are no competing interests with this manuscript.
Databáze:	MEDLINE
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