Exp Clin Endocrinol Diabetes 2007; 115 - P02_118
DOI: 10.1055/s-2007-972525

Expression of placental growth factor–1 (PlGF-1) in synovial tissue from rheumatoid arthritis (RA) patients: Role on inflammation and on DHEAS to DHEA conversion

S Capellino 1, G Schiechl 1, C Weidler 1, S Anders 2, CGO Baerwald 3, F Buttgereit 4, R Straub 1
  • 1University Hospital Regensburg, Dept. of Internal Medicine I, Regensburg, Germany
  • 2Bavarian Red Cross Hospital, Dept. of Orthopedic Surgery, Bad Abbach, Germany
  • 3University Hospital Leipzig, Dept. of Internal Medicine IV, Leipzig, Germany
  • 4Charité University Hospital, Dept. of Rheumatology and Clinical Immunology, Berlin, Germany

Background: Proliferating synovial pannus is in many aspects similar to placental tissue: both are fibroblast-rich tissues with high vascularity but rare sympathetic innervation, and demonstrate strong conversion from androgenic prehormones to downstream estrogens. Furthermore, they both present neoangiogenesis, hypoxia and release of hypoxia-inducible factors such as VEGF. Interestingly, we found PlGF expression in synovial fluid of rheumatoid arthritis (RA) patients.

Objectives: As PlGF is present in synovial fluid of RA patients, the aim was to investigate the role of PlGF-1 in RA synovial tissue, and to compare the effects in this pathology with its role in the placenta.

Materials and methods: 30 RA and 50 osteoarthritis (OA) patients were in the focus of this study. To investigate the presence of PlGF-1 in synovial tissue and the PlGF-1+ cells, immunohistochemistry and immunofluorescence were used. To determine the conversion of DHEAS to DHEA, synovial cells were cultured with [3H]DHEAS for 24 hours. The supernatants were than analyzed by thin layer chromatography (TLC) to detect the concentration of [3H]DHEA after conversion from [3H]DHEAS.

Results: PlGF-1+ cells were detected in both RA and OA patients with a similar cellular density. PlGF-1+ cells were macrophages. In both disease groups, density of PlGF-1+ cells was higher in male than in female patients and correlated with density of macrophages. Interestingly, only in OA synovial cell culture the concentration of [3H]DHEA after conversion from [3H]DHEAS was significantly correlated to density of PlGF-1+ cells.

Conclusions: PlGF-1 in inflamed synovium plays similar roles as compared to its function in the placenta: It is related to vessel formation and, in OA patients, to androgen / estrogen conversion. Therefore we suppose that evolutionarily conserved functions of PlGF-1 are present in the inflammatory response in different pathologies.