Investigation of the Tumorsupressor Genes P53 and NM23 in Synovial Membranes of Patients with Rheumatoid Arthritis

Journal/Book: Z Rheumatol 1998; 57 Suppl. 1: 51 (P 24). 1998;

Abstract: Robert-Rössle Klinik Labor für Gentherapie; 1Institut für Pathologie Universitätsklinikum Leipzig Introduction: Abnormal expression of oncogenes seem to be involved in the pathogenesis of rheumatoid arthritis (RA) by induction of fibroblast proliferation and production of lysosomal enzymes. Material and Methods: We investigated the expression of p53 and nm23 tumor suppressor genes with semiquantitative RT-PCR and immunohistochemistry in synovial membranes (SM) of patients with RA (n = 8) in synovium with other inflammatory joint disease (n = 8) and in 5 synovial membranes without pathological features (nSM). For RT-PCR RNA was isolated with a modified method of Chomszinski/Sacchie followed by DNAse digestion and additional transcription of total RNA into cDNA. The cDNA's from the synovial tissue were adjusted for an equal amplification level with the "house keeping" gene GAPDH and with semiquantitive PCR we determined the relativ gene expression. Immunhistochemistry was performed with ABC-method. Results: The mRNA level of p53 showed no significant difference between probes. Nm23 was significantly increased in synovial tissue of patients with RA compared with SM of other inflammatory joint disease. lmmunohistochemistry studies on paraffin-embedded synovial tissue using mAk DO-7 (Novo Castra) showed no immunoreactivity for wild type and mutant p53. Immunhistochemical staining for nm23 with mAK NCL-nm23 (Novo Castra) revealed a strong reaction in cytoplasm of plasma cells. Conclusion: These findings confirm that p53 does not play the same specific role in RA as in neoplastic disease. The functional significance of nm23 needs further investigations. le

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