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Platelet-rich plasma counteracts interleukin-1 induced inhibition of collagen biosynthesis through recovery of impaired β1-integrin signaling and prolidase activity in human skin fibroblasts.

Although inflammation is the first step in wound healing, it contributes to down-regulation of collagen biosynthesis delaying the process of tissue regeneration. The study was conducted to evaluate the effects of platelet-rich plasma (PRP) on interleukin-1β (IL-1β) – dependent inhibition of collagen synthesis, prolidase activity, and β1-integrin signaling in cultured human skin fibroblasts. PRP was obtain using the SmartPReP®2 Autologous Platelet Concentrate+ System. Collagen biosynthesis and prolidase activity were measured in confluent human skin fibroblast cultures with IL-1β, PRP, hyaluronic acid (HA), and mixtures of IL-1β with PRP or HA. Immunofluorescence bioimaging analysis was employed to evaluate expression of β1 integrin receptor, cyclooxygenase-2 (COX-2) and nuclear factor-κB (NF-κB) protein. Incubation of fibroblasts with 2% PRP for 24 h contributed to about 500% increase in collagen biosynthesis and a significant increase in the expression of β1-integrin receptor and prolidase activity, compared to the control cells. In the cells treated with IL-1β, collagen biosynthesis, β1-integrin receptor expression, and prolidase activity were decreased while COX-2 and NF-κB expressions were significantly increased. All these processes were recovered to control values by PRP or HA; however, PRP was found to act more effectively than HA. It was found that PRP counteracted IL-1β -dependent inhibition of collagen synthesis through recovery of β1-integrin receptor expression and prolidase activity and down-regulation of COX-2 and NF-κB expressions in cultured fibroblasts. The data suggest that PRP evoke anti-inflammatory activity that is desirable in tissue regeneration.