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Background   Mesenchymal stem cells (MSCs) emerged as a promising therapy for tendon pathologies. Microfragmented adipose tissue ( μ FAT) represents a convenient autologous product for the application of MSC-based therapies in the clinical setting. In the present study, the ability of  μ FAT to counteract inflammatory processes induced by IL-1 β  on human tendon cells (TCs) was evaluated.Methods   Cell viability and proliferation were evaluated after 48 hours of transwell coculture of TCs and autologous  μ FAT in the presence or absence of IL-1 β . Gene expression of scleraxis, collagen type I and type III, metalloproteinases-1 and -3, and cyclooxygenase-2 was evaluated by real-time RT-PCR. The content of VEGF, IL-1Ra, TNF α , and IL-6 was evaluated by ELISA.Results   IL-1 β -treated TCs showed augmented collagen type III, metalloproteases, and cyclooxygenase-2 expression.  μ FAT was able to reduce the expression of collagen type III and metalloproteases-1 in a significant manner, and at the same time, it enhanced the production of VEGF, IL-1Ra, and IL-6.Conclusions   In this in vitro model of tendon cell inflammation, the paracrine action of  μ FAT, exerted by anti-inflammatory molecules and growth factors, was able to inhibit the expression of fibrosis and catabolic markers. Then, these results suggest that the application of  μ FAT may represent an effective conservative or adjuvant therapy for the treatment of tendon disorders.

Autologous Microfragmented Adipose Tissue Reduces the Catabolic and Fibrosis Response in an In Vitro Model of Tendon Cell Inflammation