Figure 5

Proposed model of plasma gelsolin (pGSN) function in clearing actin from synovial joints of rheumatoid arthritis patients with acute joint effusion. (1) pGSN and other proteins from blood enter the inflamed synovial joint space freely due to increased permeability. (2) Actin is exposed to the extracellular environment of the joint because of tissue cell damage. pGSN gets soaked up in the exposed actin networks because of its high affinity for actin. (3) Actin filaments (F-actin) are severed by pGSN and GSN-F-actin complexes released to the synovial fluid (SF). (4) pGSN caps the barbed ends of the filaments, preventing polymerization from the fast-growing ends. Due to the presence of Gc-globulin [43], the pool of free actin monomers in SF is likely to be low, favoring depolymerization from the pointed (slow-growing) ends of the actin filaments. (5) Actin monomers released from the filaments are bound by Gc-globulin, which (6) efficiently clears it in the liver [18]. G-actin, monomeric actin.