Aberrant production of gliostatin/platelet-derived endothelial cell growth factor in rheumatoid synovium.

OBJECTIVE To purify a protein inhibitor from rheumatoid arthritis (RA) synovial fluids which suppresses the apparent incorporation of 3H-thymidine into fibroblasts and synovial cells, and to define its biochemical features that have clinical relevance to the pathogenesis of RA. METHODS Several standard chromatographic techniques were employed for the purification of the protein. Immunochemical methods with monoclonal antibody were used to quantify and visualize the protein in sera, synovial fluids, and tissues from RA patients. RESULTS The chemical properties of purified inhibitor from RA synovial fluids confirmed its identity as gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF), a potent angiogenic factor. The gliostatin/PD-ECGF level in synovial fluid and serum was higher in RA patients than in osteoarthritis controls. CONCLUSION These findings strongly suggest that gliostatin/PD-ECGF might play an important role in the aberrant neovascularization of rheumatoid synovium.

[1]  K. Nakanishi,et al.  Neurotrophic action of gliostatin on cocultured neurons with glial cells , 1993, Brain Research.

[2]  T. Kato,et al.  Establishment of an enzyme immunoassay system for gliostatin/platelet-derived endothelial cell growth factor (PD-ECGF). , 1993, Biochimica et biophysica acta.

[3]  N. Dodsworth,et al.  Thymidine phosphorylase activity of platelet-derived endothelial cell growth factor is responsible for endothelial cell mitogenicity. , 1993, European journal of biochemistry.

[4]  R. Bicknell,et al.  Expression of platelet-derived endothelial cell growth factor in Escherichia coli and confirmation of its thymidine phosphorylase activity. , 1992, Biochemistry.

[5]  K. Nakanishi,et al.  Neurotrophic action of gliostatin on cortical neurons. Identity of gliostatin and platelet-derived endothelial cell growth factor. , 1992, The Journal of biological chemistry.

[6]  K. Nakanishi,et al.  A Novel Glial Growth Inhibitory Factor, Gliostatin, Derived from Neurofibroma , 1992, Journal of neurochemistry.

[7]  K. Miyazono,et al.  Platelet-derived endothelial cell growth factor has thymidine phosphorylase activity. , 1992, Biochemical and biophysical research communications.

[8]  K. Nakanishi,et al.  von Recklinghausen neurofibroma produces neuronal and glial growth-modulating factors , 1991, Brain Research.

[9]  C. Heldin,et al.  Characterization of platelet-derived growth factor beta-receptor expressing cells in the vasculature of human rheumatoid synovium. , 1991, Laboratory investigation; a journal of technical methods and pathology.

[10]  D. Bani,et al.  Interleukin 1 is an autocrine regulator of human endothelial cell growth. , 1990, Proceedings of the National Academy of Sciences of the United States of America.

[11]  K. Shiozawa,et al.  Human epidermal growth factor for the stratification of synovial lining layer and neovascularisation in rheumatoid arthritis. , 1989, Annals of the rheumatic diseases.

[12]  D. Rifkin,et al.  Recent developments in the cell biology of basic fibroblast growth factor , 1989, The Journal of cell biology.

[13]  K. Miyazono,et al.  Identification of angiogenic activity and the cloning and expression of platelet-derived endothelial cell growth factor , 1989, Nature.

[14]  J. Symons,et al.  CORRELATION OF PLASMA INTERLEUKIN 1 LEVELS WITH DISEASE ACTIVITY IN RHEUMATOID ARTHRITIS , 1988, The Lancet.

[15]  N. Miyasaka,et al.  Augmented interleukin-1 production and HLA-DR expression in the synovium of rheumatoid arthritis patients. Possible involvement in joint destruction. , 1988, Arthritis and rheumatism.

[16]  M. Liang,et al.  The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis. , 1988, Arthritis and rheumatism.

[17]  Y. Shimosato,et al.  The AMeX method. A simplified technique of tissue processing and paraffin embedding with improved preservation of antigens for immunostaining. , 1986, The American journal of pathology.

[18]  T. Joh,et al.  Physiological concentrations of human epidermal growth factor in biological fluids: use of a sensitive enzyme immunoassay. , 1986, Clinica chimica acta; international journal of clinical chemistry.

[19]  E. Ishikawa,et al.  More useful maleimide compounds for the conjugation of Fab' to horseradish peroxidase through thiol groups in the hinge. , 1984, Journal of applied biochemistry.

[20]  C. Brinckerhoff.  Morphologic and mitogenic responses of rabbit synovial fibroblasts to transforming growth factor β require transforming growth factor α or epidermal growth factor , 1983 .

[21]  S. Kumar,et al.  Relationship of angiogenesis factor in synovial fluid to various joint diseases. , 1983, Annals of the rheumatic diseases.

[22]  S. Hsu,et al.  Use of avidin-biotin-peroxidase complex (ABC) in immunoperoxidase techniques: a comparison between ABC and unlabeled antibody (PAP) procedures. , 1981, The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society.

[23]  M. Piazza,et al.  HEPATITIS B NOT TRANSMISSIBLE VIA FÆCAL-ORAL ROUTE , 1975, The Lancet.

[24]  U. K. Laemmli,et al.  Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4 , 1970, Nature.

[25]  L. Levine,et al.  Differentiated Rat Glial Cell Strain in Tissue Culture , 1968, Science.

[26]  A. Yoshimura,et al.  Angiogenic factor , 1992, Nature.

[27]  M. Sporn,et al.  Cytokines and growth regulation of synoviocytes from patients with rheumatoid arthritis and rats with streptococcal cell wall arthritis. , 1990, Growth factors.