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TYPE III COLLAGEN REGULATES MATRIX ARCHITECTURE AND MECHANOSENSING DURING WOUND HEALING.
Stewart, Daniel C; Brisson, Becky K; Yen, William K; Liu, Yuchen; Wang, Chao; Ruthel, Gordon; Gullberg, Donald; Mauck, Robert L; Maden, Malcolm; Han, Lin; Volk, Susan W.
Afiliación
  • Stewart DC; Department of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Brisson BK; Department of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Yen WK; Department of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Liu Y; School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA 19104, USA.
  • Wang C; School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA 19104, USA.
  • Ruthel G; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
  • Gullberg D; Department of Biomedicine and Centre for Cancer Biomarkers (CCBIO), Norwegian Centre of Excellence, University of Bergen, Bergen, Norway.
  • Mauck RL; Department of Bioengineering, University of Pennsylvania, Philadelphia, PA 19104, USA; McKay Orthopaedic Research Laboratory, Department of Orthopaedic Surgery, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Translational Musculoskeletal Research Center, Corpor
  • Maden M; Department of Biology, College of Liberal Arts and Sciences, University of Florida, Gainesville, FL 32611, USA.
  • Han L; School of Biomedical Engineering, Science and Health Systems, Drexel University, Philadelphia, PA 19104, USA.
  • Volk SW; Department of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA. Electronic address: swvolk@vet.upenn.edu.
J Invest Dermatol ; 2024 Sep 03.
Article en En | MEDLINE | ID: mdl-39236902
ABSTRACT
Post-natal cutaneous wound healing is characterized by development of collagen-rich scar lacking the architecture and functional integrity of unwounded tissue. Directing cell behaviors to efficiently heal wounds while minimizing scar formation remains a major wound management goal. Herein, we demonstrate type III collagen (Col3) as a critical regulator of re-epithelialization and scar formation during healing of Col3-enriched, regenerative (Acomys), scar-permissive (CD-1 Mus and wild-type Col3B6/B6 mice), and Col3-deficient, scar-promoting (Col3F/F, a murine conditional knockdown model) cutaneous wound models. We define a scar-permissive fibrillar collagen architecture signature characterized by elongated and anisotropically-aligned collagen fibers that is dose-dependently suppressed by Col3. Further, loss of Col3 alters how cells interpret their microenvironment - their mechanoperception - such that Col3-deficient cells display mechanically-active phenotypes in the absence of increased microenvironmental stiffness via upregulation and engagement of the profibrotic integrin α11. Further understanding Col3's role in regulating matrix architecture and mechanoresponses may inform clinical strategies that harness pro-regenerative mechanisms.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Invest Dermatol Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: J Invest Dermatol Año: 2024 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Estados Unidos