Platelet-Released Growth Factors Modulate the Secretion of Cytokines in Synoviocytes under Inflammatory Joint Disease

Author:

Tohidnezhad Mersedeh1ORCID,Bayer Andreas2ORCID,Rasuo Biljana1,Hock Jennifer Vanessa Phi1,Kweider Nisreen1,Fragoulis Athanassios1,Sönmez Tolga Taha134,Jahr Holger5,Pufe Thomas1,Lippross Sebastian6

Affiliation:

1. Institute of Anatomy and Cell Biology, Medical Faculty, RWTH Aachen University, Wendlingweg 2, 52074 Aachen, Germany

2. Department of Heart and Vascular Surgery, University Hospital of Schleswig-Holstein, Kiel, Germany

3. Department of Oral, Cranio-Maxillofacial and Facial Plastic Surgery, Hospital Karlsruhe of University Freiburg, Karlsruhe, Germany

4. Frankfurt Orofacial Regenerative Medicine-Lab (FORM), University Hospital Frankfurt Goethe University, Frankfurt am Main, Germany

5. Department of Orthopaedic Surgery, RWTH Aachen University, Pauwelsstr. 30, 52074 Aachen, Germany

6. Department of Traumatology, University Hospital of Schleswig-Holstein, Kiel, Germany

Abstract

The etiology and pathogenesis of rheumatoid arthritis (RA) are marked by a complex interplay of various cell populations and is mediated by different signaling pathways. Traditionally, therapies have primarily focused on pain relief, reducing inflammation and the recovery of joint function. More recently, however, researchers have discussed the therapeutic efficacy of autologous platelet-rich plasma (PRP). The main objective of this work is to examine the influences of platelet-released growth factor (PRGF) on human synoviocytes under inflammatory conditions. Additionally, it is checked to which extend treatment with platelet concentrate influences the release of cytokines form synoviocytes. For this purpose, an in vitro RA model was created by stimulating the cells with the TNF-α. The release of cytokines was measured by ELISA. The cytokine gene expression was analyzed by real-time PCR. It has been observed that the stimulation concentration of 10 ng/ml TNF-α resulted in a significantly increased endogenous secretion and gene expression of IL-6 and TNF-α. The anti-inflammatory effect of PRGF could be confirmed through significant reduction of TNF-α and IL-1β. An induced inflammatory condition seems to cause PRGF to inhibit the release of proinflammatory cytokines. Further study is required to understand the exact effect mechanism of PRGF on synoviocytes.

Funder

Merck Sharp and Dohme

Publisher

Hindawi Limited

Subject

Cell Biology,Immunology

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