PLATELET-RICH PLASMA COUNTERACTS INTERLEUKIN-1 INDUCED INHIBITION OF COLLAGEN BIOSYNTHESIS THROUGH RECOVERY OF IMPAIRED Beta 1-INTEGRIN SIGNALING AND PROLIDASE ACTIVITY IN HUMAN SKIN FIBROBLASTS

Although inflammation is the first step in wound healing, it contributes to the down-regulation of collagen biosynthesis delaying the process of tissue regeneration. The study was conducted to evalu-ate the effects of platelet-rich plasma (PRP) on interleukin-10 (IL-10) - dependent inhibition of colla-gen synthesis, prolidase activity, and 01-integrin signaling in cultured human skin fibroblasts. PRP was obtained using the SmartPReP (R) 2 Autologous Platelet Concentrate+ System. Collagen biosynthesis and prolidase activity were measured in confluent human skin fibroblast cultures with IL-10, PRP, hyaluronic acid (HA), and mixtures of IL-10 with PRP or HA. Immunofluorescence bioimaging analysis was em-ployed to evaluate the expression of 01 integrin receptor, cyclooxygenase-2 (COX-2), and nuclear factor-kappa B (NF-kappa B) protein. Incubation of fibroblasts with 2% PRP for 24 h contributed to about a 500% increase in collagen biosynthesis and a significant increase in the expression of 01-integrin receptor and prolidase activity, compared to the control cells. In the cells treated with IL-10, collagen biosynthesis, 01-integrin receptor expression, and prolidase activity were decreased while COX-2 and NF-kappa B 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-10-dependent inhibi-tion of collagen synthesis through the recovery of 01-integrin receptor expression and prolidase activity and down-regulation of COX-2 and NF-kappa B expressions in cultured fibroblasts. The data suggest that PRP evokes anti-inflammatory activity that is desirable in tissue regeneration.