PGE2, PGF2 alpha, and TXB2 biosynthesis by human rheumatoid synovia.
Prostaglandins (PG) are currently suspected to be involved in human rheumatoid arthritis (RA). We have studied the PG [PGE2, PGF2 alpha, and Thromboxane B2 (TXB2)] biosynthesis capacity of normal (from amputations) and pathologic (osteoarthritis (OA) and RA) synovia. The measurement is done on the whole homogenate and microsomal fraction after 40 min incubation, without exogenous arachidonic acid (AA) or with a saturating concentration (25 micrograms/ml) of this compound, using a radioimmunoassay method. There is a considerable increase in PGE2 and PGF2 alpha production by the rheumatoid synovia and more PGE2 and PGF2 alpha are formed. This production is more marked for homogenates than microsomal fraction. The OA group is not homogeneous and does not differ significantly either from normals or from RA. The addition of AA considerably increases the biosynthesis of PG in both normal and pathologic tissue. For TXB2, the first results (four synovia) show no or a small biosynthesis in RA as well as in normals. Nevertheless, the levels before incubation seem higher in RA than in normal tissue.
D001095:Arachidonic Acids / Q000378:metabolism; D001172:Arthritis, Rheumatoid / Q000378:metabolism*; D006801:Humans; D008861:Microsomes / Q000378:metabolism; D010003:Osteoarthritis / Q000378:metabolism; D011458:Prostaglandins E / Q000096:biosynthesis*; D011460:Prostaglandins F / Q000096:biosynthesis*; D013583:Synovial Membrane / Q000378:metabolism*; D013929:Thromboxane B2 / Q000096:biosynthesis*; D013931:Thromboxanes / Q000096:biosynthesis*
D001095:Arachidonic Acids; D011458:Prostaglandins E; D011460:Prostaglandins F; D013931:Thromboxanes; D013929:Thromboxane B2