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We have previously found an increased mast cell density in tendon biopsies from patients with patellar tendinopathy compared to controls. This study examined the influence of mast cells on basic tenocyte functions, including production of the inflammatory mediator prostaglandin E2 (PGE 2 ), extracellular matrix remodeling and matrix metalloproteinase (MMP) gene transcription, and collagen synthesis.    Methods  Primary human tenocytes were stimulated with an established human mast cell line (HMC-1). Extracellular matrix remodeling was studied by culturing tenocytes in a three-dimensional collagen lattice. Survival/proliferation was assessed with the 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium salt (MTS) assay. Levels of mRNA for  COX-2, COL1A1, MMP1 , and  MMP7  were determined by quantitative real-time polymerase chain reaction (qPCR). Cox-2 protein level was assessed by Western blot analysis and type I procollagen was detected by immunofluorescent staining. PGE 2  levels were determined using an enzyme-linked immunosorbent assay (ELISA).    Results  Mast cells stimulated tenocytes to produce increased levels of COX-2 and the pro-inflammatory mediator PGE 2 , which in turn decreased  COL1A1  mRNA expression. Additionally, mast cells reduced the type I procollagen protein levels produced by tenocytes. Transforming growth factor beta 1 (TGF-β1) was responsible for the induction of Cox-2 and PGE 2  by tenocytes. Mast cells increased  MMP1  and  MMP7  transcription and increased the contraction of a three-dimensional collagen lattice by tenocytes, a phenomenon which was blocked by a pan-MMP inhibitor (Batimastat).    Conclusion  Our data demonstrate that mast cell-derived PGE 2  reduces collagen synthesis and enhances expression and activities of MMPs in human tenocytes.

Mast cells exert pro-inflammatory effects of relevance to the pathophyisology of tendinopathy