English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Tools annual

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Presents the access of premium content as premium feature

Premium Content

Global: Zendy Plus annual

Global: Zendy Free Plan

Flexor tendon injuries heal with excessive scar tissue that limits range of motion and increases incidence of re-rupture. The molecular mechanisms that govern tendon healing are not well defined. Both the canonical nuclear factor kappa B (NF-κB) and mitogen activated protein kinase (MAPK) pathways have been implicated in tendon healing. The gene  NFKB1  (proteins p105/p50) is involved in both NF-κB and MAPK signaling cascades. In the present study, we tested the hypothesis that global  NFKB1  deletion would increase activation of both NF-κB and MAPK through loss of signaling repressors, resulting in increased matrix deposition and altered biomechanical properties. As hypothesized,  NFKB1  deletion increased activation of both NF-κB and MAPK signaling. While gliding function was not affected,  NFKB1  deletion resulted in tendons that were significantly stiffer and trending towards increased strength by four weeks post-repair.  NFKB1  deletion resulted in increased collagen deposition, increase macrophage recruitment, and increased presence of myofibroblasts. Furthermore,  NFKB1  deletion increased expression of matrix-related genes ( Col1a1 ,  Col3a1 ), macrophage-associated genes ( Adgre1 ,  Ccl2 ), myofibroblast markers ( Acta2 ), and general inflammation ( Tnf ). Taken together, these data suggest that increased activation of NF-κB and MAPK via  NFKB1  deletion enhance macrophage and myofibroblast content at the repair, driving increased collagen deposition and biomechanical properties.

Deletion of NFKB1 enhances canonical NF-κB signaling and increases macrophage and myofibroblast content during tendon healing