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Embryonic and postnatal tendon cells respond differently to interleukin‐1β
Author(s) -
Li Jiewen,
Stoppato Matteo,
Schiele Nathan R.,
Graybeal Kaori L.,
Nguyen Phong K.,
Kuo Catherine K.
Publication year - 2019
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/nyas.14013
Subject(s) - embryonic stem cell , microbiology and biotechnology , inflammation , p38 mitogen activated protein kinases , tendon , proinflammatory cytokine , mapk/erk pathway , matrix metalloproteinase , biology , signal transduction , immunology , medicine , anatomy , biochemistry , gene
Adult tendons heal as scar tissue, whereas embryonic tendons heal scarlessly via unknown mechanisms. Scarred tendon healing results from inflammation‐driven imbalances in anabolic and catabolic functions. To test scarless versus scarring age tendon cell responses to inflammatory conditions, we treated embryonic and postnatal tendon cells with interleukin (IL)‐1β and characterized expression of collagens, matrix metalloproteinases (MMPs), inflammatory mediators, and phosphorylation of signaling molecules. At baseline, postnatal cells expressed significantly higher levels of inflammatory mediators. When treated with IL‐1β, both postnatal and embryonic cells upregulated inflammatory mediators and MMPs. Notably, postnatal cells secreted inflammatory factors up to 12.5 times the concentration in embryonic cultures. IL‐1β activated NF‐κB p65 and p38 mitogen‐activated protein kinase (MAPK) pathways in both cell types, but phosphorylated p38 MAPK levels were two times higher in postnatal than embryonic cells. Our results suggest that scarred healing tendon cells respond to proinflammatory cytokines by promoting an imbalance in anabolic and catabolic functions, and that the heightened response involves p38 MAPK signaling activity. In contrast, embryonic cell responses are smaller in magnitude. These intriguing findings support a potential role for tendon cells in determining scarless versus scarred healing outcomes by regulating the balance between anabolic and catabolic functions during tendon healing.