INCREASED PHOSPHATE CONTENT IN COMPLEMENT COMPONENT C3, FIBRINOGEN, VITRONECTIN, AND OTHER PLASMAPROTEINS IN SYSTEMIC LUPUS-ERYTHEMATOSUS -COVARIATION WITH PLATELET ACTIVATION AND POSSIBLE ASSOCIATION WITH THROMBOSIS

Objective. To investigate whether extracellular phosphorylation of pla sma proteins takes place in vivo in patients with systemic lupus eryth ematosus (SLE), to determine possible correlations between phosphate l evels and clinical and/or laboratory parameters, and to identify indiv idual phosphorylated plasma proteins. Methods. Sera from SLE patients were analyzed for total amounts of protein-bound phosphate by a colori metric technique, and for levels of beta-thromboglobulin by radioimmun oassay, In addition, the ability of these sera to activate platelets, resulting in the release of protein kinase, was tested using an assay in which platelet-rich plasma from healthy blood donors was incubated with sera or immune complexes from SLE patients, In this assay, [gamma -P-32]ATP was added, and P-32-labeled C3 was quantified, Phosphate in individual proteins was detected by Western blot analysis. Results. P- 32-labeled, activated platelets were able to phosphorylate exogenously added proteins, without the addition of ATP or cations, Platelet-rich plasma from healthy blood donors became activated by sera of by polye thylene glycol-precipitated immune complexes from patients with SLE, w hich led to the extracellular phosphorylation of plasma proteins, exem plified in the C3 assay, The phosphate content in plasma proteins was increased in SLE patients with previous thrombosis, The degree of phos phorylation increased up to 3-fold in serial samples obtained from 2 S LE patients during periods of disease exacerbation, Substantial phosph ate increases were seen in C3 and fibrinogen, The changes were linked to platelet activation because of the observed covariation with the le vels of beta-thromboglobulin. Conclusion. In SLE patients, the phospha te content in plasma proteins (including C3 and fibrinogen) increases due to platelet activation.