Platelet-released growth factors enhance the secretion of hyaluronic acid and induce hepatocyte growth factor production by synovial fibroblasts from arthritic patients

• Published in: Rheumatology (Oxford, England) England), 2007-12, Vol.46 (12), p.1769-1772
• Main Authors: Anitua, E., Sánchez, M., Nurden, A. T., Zalduendo, M. M., de la Fuente, M., Azofra, J., Andía, I.
• Format: Article
• Language: English
• Subjects: Aged; Biological and medical sciences; Bones, joints and connective tissue. Antiinflammatory agents; Cells, Cultured; Diseases of the osteoarticular system; Female; Fibroblasts - drug effects; Fibroblasts - physiology; Growth factors; Hepatocyte Growth Factor - metabolism; Humans; Hyaluronic Acid - secretion; IL-β; Interleukin-1beta - pharmacology; Male; Medical sciences; Middle Aged; Miscellaneous. Osteoarticular involvement in other diseases; Osteoarthritis; Osteoarthritis - drug therapy; Osteoarthritis - pathology; Pharmacology. Drug treatments; Platelet-rich plasma; Probability; Sensitivity and Specificity; Statistics, Nonparametric; Synovial cells; Synovial Membrane - cytology; Thymidine Phosphorylase - pharmacology; Transforming Growth Factor beta1 - pharmacology; Vascular Endothelial Growth Factor A - pharmacology
• ISSN: 1462-0324; 1462-0332
• DOI: 10.1093/rheumatology/kem234

Objectives. Autologous platelet-secreted growth factors (GFs) may have therapeutic effects in osteoarthritis (OA) capsular joints via multiple mechanisms. Our aim was to examine the effect of a platelet-derived preparation rich in growth factors (PRGFs) in OA synovial cell biology. Methods. Synovial cells were isolated from 10 osteoarthritic patients and cultured in serum-free media (basal conditions) and exposed to either a platelet-poor preparation or PRGF for 72 h. Cells activated with interleukin-1β (IL-1β) for 48 h were also exposed to PRGF. Changes in several events relevant to joint homeostasis including (i) hyaluronic acid (HA) secretion, (ii) the balance between metalloproteinase-1, -3 and -13 (MMP-1, MMP-3 and MMP-13) and tissue inhibitor-1 (TIMP-1) and (iii) the secretion of transforming growth factor-β1(TGF-β1), vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF), were all assessed. Results. PRGF significantly enhanced HA secretion compared with platelet-poor preparations, P < 0.05; at the same time release of TIMP-1, MMP-1, MMP-3 and MMP-13 were not affected. An increased HGF production was observed (P < 0.05) but VEGF and TGF-β1 levels remained unchanged. PRGF significantly enhanced the secretion of HA induced by IL-1β activation, P < 0.05, but it did not modify the IL-1β-induced rise in MMP-1, MMP-3 and VEGF. In contrast, PRGF-induced HGF production was abolished by the presence of IL-1β during PRGF treatment, P < 0.05. Conclusions. Intra-articular administration of PRGF might be beneficial in restoring HA concentration and switching angiogenesis to a more balanced status but does not halt the effects of IL-1β on synovial cells.