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Partial Tendon Injury at the Tendon-to-Bone Enthesis Activates Skeletal Stem Cells.
Titan, Ashley L; Davitt, Michael; Foster, Deshka; Salhotra, Ankit; Menon, Siddharth; Chen, Kellen; Fahy, Evan; Lopez, Michael; Jones, R Ellen; Baiu, Ioana; Burcham, Austin; Januszyk, Michael; Gurtner, Geoffrey; Fox, Paige; Chan, Charles; Quarto, Natalina; Longaker, Michael.
Affiliation
  • Titan AL; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Davitt M; Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Foster D; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Salhotra A; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Menon S; Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Chen K; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Fahy E; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Lopez M; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Jones RE; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Baiu I; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Burcham A; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Januszyk M; Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Gurtner G; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Fox P; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Chan C; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Quarto N; Department of Surgery, Stanford University School of Medicine, Stanford, CA, USA.
  • Longaker M; Hagey Laboratory for Pediatric Regenerative Medicine, Department of Surgery, Division of Plastic and Reconstructive Surgery, Stanford University School of Medicine, Stanford, CA, USA.
Stem Cells Transl Med ; 11(7): 715-726, 2022 07 20.
Article in En | MEDLINE | ID: mdl-35640155
ABSTRACT
The tendon enthesis plays a critical role in facilitating movement and reducing stress within joints. Partial enthesis injuries heal in a mechanically inferior manner and never achieve healthy tissue function. The cells responsible for tendon-to-bone healing remain incompletely characterized and their origin is unknown. Here, we evaluated the putative role of mouse skeletal stem cells (mSSCs) in the enthesis after partial-injury. We found that mSSCs were present at elevated levels within the enthesis following injury and that these cells downregulated TGFß signaling pathway elements at both the RNA and protein levels. Exogenous application of TGFß post-injury led to a reduced mSSC response and impaired healing, whereas treatment with a TGFß inhibitor (SB43154) resulted in a more robust mSSC response. Collectively, these data suggest that mSSCs may augment tendon-to-bone healing by dampening the effects of TGFß signaling within the mSSC niche.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Tendon Injuries / Tendons Limits: Animals Language: En Journal: Stem Cells Transl Med Year: 2022 Document type: Article Affiliation country:
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Tendon Injuries / Tendons Limits: Animals Language: En Journal: Stem Cells Transl Med Year: 2022 Document type: Article Affiliation country: