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CD200 as a Potential New Player in Inflammation during Rotator Cuff Tendon Injury/Repair: An In Vitro Model.
Raffaella Giancola1, Francesco Oliva2,3, Marialucia Gallorini4
1Department of Haematology, Transfusion Medicine and Biotechnologies, Cytofluorimetry and Cell Sorting Service, Ospedale Spirito Santo, 65122 Pescara, Italy.
International Journal of Molecular Sciences
|December 11, 2022
Summary
Tumor necrosis factor-alpha (TNFα) and interferon-gamma (IFNγ) alter rotator cuff tendon stem cell (TCSC) populations and upregulate CD200. These findings suggest CD200 may regulate inflammation in tendon injuries.
Area of Science:
- Biomedical Engineering
- Stem Cell Biology
- Musculoskeletal Research
Background:
- Rotator cuff tendon (RCT) disease involves inflammation, with pro-inflammatory cytokines and tendon stem/progenitor cells (TSPCs) playing key roles.
- The precise molecular mechanisms underlying RCT inflammation remain incompletely understood.
Purpose of the Study:
- To investigate the effects of pro-inflammatory cytokines on rotator cuff tendon stem/progenitor cells (TSPCs).
- To identify molecular players involved in the inflammatory response within TSPCs.
Main Methods:
- Flow cytometry was used to analyze subpopulations of TSPCs after TNFα and/or IFNγ administration.
- Protein expression of STAT1, STAT3, and MMP9 was assessed.
- Gene expression of IRF1, CAAT, DOK2, NF-κb, TGFBR2, and RAS-GAP was analyzed.
Main Results:
- TNFα alone or with IFNγ decreased CD146+CD49d+ and CD146+CD49f+ TSPCs but not CD146+CD109+ TSPCs.
- Pro-inflammatory cytokines upregulated CD200 expression in CD146+ TSPCs.
- The TNFα/IFNγ combination modulated STAT1, STAT3, MMP9, IRF1, CAAT, and DOK2 expression.
Conclusions:
- CD200 may have a significant role in regulating inflammation associated with tendon injuries.
- Specific genes like IRF1, CAAT, and DOK2 could be novel contributors to TSPC inflammatory responses.
