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Macrophage depletion impairs neonatal tendon regeneration
Author(s) -
Howell Kristen L.,
Kaji Deepak A.,
Li Thomas M.,
Montero Angela,
Yeoh Kenji,
Nasser Philip,
Huang Alice H.
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202100049r
Subject(s) - tendon , regeneration (biology) , inflammation , macrophage , wound healing , immune system , microbiology and biotechnology , downregulation and upregulation , connective tissue , biology , immunology , chemotaxis , medicine , pathology , anatomy , gene , receptor , in vitro , biochemistry
Tendons are dense connective tissues that transmit muscle forces to the skeleton. After adult injury, healing potential is generally poor and dominated by scar formation. Although the immune response is a key feature of healing, the specific immune cells and signals that drive tendon healing have not been fully defined. In particular, the immune regulators underlying tendon regeneration are almost completely unknown due to a paucity of tendon regeneration models. Using a mouse model of neonatal tendon regeneration, we screened for immune‐related markers and identified upregulation of several genes associated with inflammation, macrophage chemotaxis, and TGFβ signaling after injury. Depletion of macrophages using AP20187 treatment of MaFIA mice resulted in impaired functional healing, reduced cell proliferation, reduced ScxGFP+ neo‐tendon formation, and altered tendon gene expression. Collectively, these results show that inflammation is a key component of neonatal tendon regeneration and demonstrate a requirement for macrophages in effective functional healing.