Mendes Mariana Trivilin, Murari-do-Nascimento Stephanie, Torrigo Isis Rossetti, Alponti Rafaela Fadoni, Yamasaki Simone Cristina, Silveira Paulo Flavio
Laboratory of Pharmacology, Instituto Butantan, Av. Vital Brasil, 1500, 05503-900 São Paulo, SP, Brazil.
Regul Pept. 2011 Apr 11;167(2-3):215-21. doi: 10.1016/j.regpep.2011.02.012. Epub 2011 Feb 13.
The objective of this study was to investigate the catalytic activity of basic aminopeptidase (APB) and its association with periarticular edema and circulating tumor necrosis factor (TNF)-alpha and type II collagen (CII) antibodies (AACII) in a rat model of rheumatoid arthritis (RA) induced by CII (CIA). Edema does not occur in part of CII-treated, even when AACII is higher than in control. TNF-alpha is detectable only in edematous CII-treated. APB in synovial membrane is predominantly a membrane-bound activity also present in soluble form and with higher activity in edematous than in non-edematous CII-treated or control. Synovial fluid and blood plasma have lower APB in non-edematous than in edematous CII-treated or control. In peripheral blood mononuclear cells (PBMCs) the highest levels of APB are found in soluble form in control and in membrane-bound form in non-edematous CII-treated. CII treatment distinguishes two categories of rats: one with arthritic edema, high AACII, detectable TNF-alpha, high soluble and membrane-bound APB in synovial membrane and low APB in the soluble fraction of PBMCs, and another without edema and with high AACII, undetectable TNF-alpha, low APB in the synovial fluid and blood plasma and high APB in the membrane-bound fraction of PBMCs. Data suggest that APB and CIA are strongly related.
