Platelet-Rich Plasma Activates Proinflammatory Signaling Pathways and Induces Oxidative Stress in Tendon Fibroblasts.
Platelet-Rich Plasma Activates Proinflammatory Signaling Pathways and Induces Oxidative Stress in Tendon Fibroblasts.
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DOI：
10.1177/0363546516637176
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发表时间：
2016-08
期刊：
影响因子：
--
通讯作者：
Mendias CL
中科院分区：
文献类型：
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作者：
Hudgens JL;Sugg KB;Grekin JA;Gumucio JP;Bedi A;Mendias CL
Tendon injuries are one of the most common musculoskeletal conditions in active patients. Platelet rich plasma (PRP) has shown some promise in the treatment of tendon disorders, but little is known as to the mechanisms by which PRP can improve tendon regeneration. PRP contains numerous different growth factors and cytokines which activate various cellular signaling cascades, but it has been difficult to determine precisely which signaling pathways and cellular responses are activated following PRP treatment. Additionally, macrophages play an important role in modulating tendon regeneration, but the influence of PRP on determining whether macrophages assume a proinflammatory or antiinflammatory phenotype remains unknown. We used genome wide expression profiling, bioinformatics and protein analysis to determine the cellular pathways activated in fibroblasts treated with PRP. We also evaluated the effect of PRP on macrophage polarization. Controlled laboratory study. Tendon fibroblasts or macrophages from rats were cultured and treated with either platelet poor plasma (PPP) or PRP. RNA or protein was isolated from cells and analyzed using microarrays, qPCR, immunoblot or bioinformatics techniques. Pathway analysis determined that the most highly induced signaling pathways in PRP treated tendon fibroblasts was the TNFα and NFκB pathways. PRP also downregulated the expression of ECM genes and induced the expression of autophagy related genes and reactive oxygen species (ROS) genes and protein markers in tendon fibroblasts. PRP failed to have a major impact on markers of macrophage polarization. PRP induces an inflammatory response in tendon fibroblasts which leads to the formation of ROS and activation of oxidative stress pathways. PRP does not appear to significantly modulate macrophage polarization. PRP might act by inducing a transient inflammatory event which could then trigger a tissue regeneration response.
