Impact of Smad3 loss of function on scarring and adhesion formation during tendon healing

Evan B. Katzel; Matthew Wolenski; Alayna E. Loiselle; Patrick Basile; Lisa M. Flick; Howard N. Langstein; Matthew J. Hilton; Hani A. Awad; Warren C. Hammert; Regis J. O'Keefe

doi:10.1002/jor.21235

journal article Sep 14, 2010

Impact of Smad3 loss of function on scarring and adhesion formation during tendon healing

Evan B. Katzel Matthew Wolenski Alayna E. Loiselle

Patrick Basile Lisa M. Flick Howard N. Langstein Matthew J. Hilton Hani A. Awad Warren C. Hammert

Regis J. O'Keefe

Journal of Orthopaedic Research Vol. 29 No. 5 pp. 684-693 · Wiley

View at Publisher Save 10.1002/jor.21235

Abstract

AbstractStudies were performed evaluating the role of Smad3, a transcription factor mediating canonical TGF‐β signaling, on scarring and adhesion formation using an established flexor digitorum longus (FDL) tendon repair model. In unoperated animals the metatarsophalangeal (MTP) range of motion (ROM) was similar in Smad3−/− and wild‐type (WT) mice while the basal tensile strength of Smad3−/− tendons was significantly (39%) lower than in WT controls. At 14 and 21 days following repair Smad3−/− MTP ROM reached approximately 50% of the basal level and was twice that observed in WT tendon repairs, consistent with reduced adhesion formation. Smad3−/− and WT maximal tensile repair strength on post‐operative day 14 was similar. However, Smad3−/− tendon repairs maximal tensile strength on day 21 was 42% lower than observed in matched WT mice, mimicking the relative decrease in strength observed in Smad3−/− FDL tendons under basal conditions. Histology showed reduced “healing callus” in Smad3−/− tendons while quantitative PCR, in situ hybridization, and immunohistochemistry showed decreased col3a1 and col1a1 and increased MMP9 gene and protein expression in repaired Smad3−/− tendons. Thus, Smad3−/− mice have reduced collagen and increased MMP9 gene and protein expression and decreased scarring following tendon FDL tendon repair. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 29:684–693, 2011

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Details

Published: Sep 14, 2010
Vol/Issue: 29(5)
Pages: 684-693
License: View

Authors

Department of Biomedical Engineering, University of Rochester, Rochester, New York 14623, United States; Center for Musculoskeletal Research, University of Rochester Medical Center, Rochester, New York 14642, United States; Department of Orthopedics & Physical Performance, University of Rochester Medical Center, Rochester, New York 14642, United States; Department of Pathology & Laboratory Medicine, University of Rochester Medical Center, Rochester, New York 14642, United States

Cite This Article

Evan B. Katzel, Matthew Wolenski, Alayna E. Loiselle, et al. (2010). Impact of Smad3 loss of function on scarring and adhesion formation during tendon healing. Journal of Orthopaedic Research, 29(5), 684-693. https://doi.org/10.1002/jor.21235

Impact of Smad3 loss of function on scarring and adhesion formation during tendon healing

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