Release kinetic of pro- and anti-inflammatory biomolecules from platelet -rich plasma and functional study on osteoarthritis synovial fibroblasts

Background aims: This study evaluated the release kinetics of numerous representative and less studied platelet - rich plasma (PRP) cytokines/chemokines with regard to the effects of various cellular compositions and incubation times. In addition, the biological effects of different PRPs on osteoarthritis synovial fibroblasts in vitro were tested. Methods: Peripheral whole blood was collected from healthy donors, and pure platelet -rich plasma (P-PRP), leukocyte -rich platelet -rich plasma (L-PRP) and platelet -poor plasma (PPP) were prepared for the analysis of the following biomolecules: IL -1 b , IL -4, IL -6, IL -10, IL -17a, IL -22, MIP-1 a /CCL-3, RANTES/CCL-5, MCP-3/CCL- 7, Gro- a /CXCL-1, PF-4/CXCL-4, ENA-78/CXCL-5, NAP-2/CXCL-7, IL-8/CXCL-8, Fractalkine/CX3CL-1, s-CD40L P-PRP, L-PRP and PPP. Their effect on osteoarthritis synovial fibroblasts in vitro was tested by analyzing changes induced in both gene expression on a panel of representative molecules involved in physiopathology of joint environment and synthesis of IL -1 b , IL -8 and hyaluronic acid. Results: This study demonstrated that among the 16 analyzed biomolecules, four were undetectable, whereas most of the detected biomolecules were more concentrated in L-PRP even when concentrations were nor- malized to platelet number. Despite the pro -inflammatory boost, the various PRP preparations did not alter synovial fibroblast gene expression of specific factors that play a pivotal role in joint tissue homeostasis and are able to induce anti-inflammatory (TIMP-1) biomolecules. Discussion: This study provides a set of reference data on the concentration and release kinetics of some less explored biomolecules that could represent potential specific effectors in the modulation of inflammatory processes and in tissue repair after treatment with PRP. ? 2020 International Society for Cell and Gene Therapy. Published by Elsevier Inc.