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Diseased and injured tendons develop fibrosis, driven by factors including TGF-β, BMPs and CTGF. IL-1β and its signal transducer Erk1/2 are known to regulate TGF-β expression in animal tendons. We utilised tissues and cells isolated from patients with shoulder tendon tears and tendons of healthy volunteers to advance understanding of how inflammation induces fibrosis in diseased human tendons. ERK1/2 expression was reduced in torn (diseased) compared to healthy patient tendon tissues. We next investigated the fibrotic responses of tendon-derived cells isolated from healthy and diseased human tendon tissues in an inflammatory milieu. IL-1β treatment induced profound ERK1/2 signalling,  TGFB1  and  BMP2  mRNA expression in diseased compared to healthy tendon-derived cells. In the diseased cells, the ERK1/2 inhibitor (PD98059) completely blocked the IL-1β-induced  TGFB1  and partially reduced  BMP2  mRNA expression. Conversely, the same treatment of healthy cells did not modulate IL-1β-induced  TGFB1  or  BMP2  mRNA expression. ERK1/2 inhibition did not attenuate IL-1β-induced  CTGF  mRNA expression in healthy or diseased tendon cells. These findings highlight differences between ERK1/2 signalling pathway activation and expression of TGF-β1 and BMP-2 between healthy and diseased tendon tissues and cells, advancing understanding of inflammation induced fibrosis during the development of human tendon disease and subsequent repair.

ERK1/2 drives IL-1β-induced expression of TGF-β1 and BMP-2 in torn tendons