RESUMO
The flexor carpi radialis brevis (FCRB) is a rare, anomalous musculotendinous structure of the wrist. Here, we report five cases of FCRB in a consecutive series of 123 distal radius fractures that were repaired by using volar locking plates.
Assuntos
Músculo Esquelético/anormalidades , Idoso , Placas Ósseas , Feminino , Antebraço , Fixação Interna de Fraturas , Humanos , Masculino , Pessoa de Meia-Idade , Fraturas do Rádio/cirurgia , Estudos RetrospectivosRESUMO
OBJECTIVE: Pentraxin 3 (PTX3) is an acute-phase reactant that is involved in amplification of the inflammatory response and innate immunity. In the present study, we evaluated the relationship between PTX3 and serum amyloid A (SAA), another acute-phase reactant, in rheumatoid synoviocytes. METHODS: PTX3 mRNA expression was examined by reverse transcription polymerase chain reaction, and PTX3 protein was measured by enzyme-linked immunosorbent assay. RESULTS: SAA induced PTX3 mRNA and PTX3 protein expression in rheumatoid synoviocytes. SAA-induced PTX3 expression was attenuated when rheumatoid synoviocytes were nucleofected with N-formyl peptide receptor ligand-1 (FPRL-1)-specific siRNA, suggesting the involvement of FPRL-1. Furthermore, SAA-induced PTX3 expression was inhibited by NF-κB or mitogen-activated protein kinase-specific inhibitors. Neither soluble TNF receptor (etanercept) nor recombinant IL-1 receptor antagonist affected PTX3 production by SAA-stimulated synoviocytes, suggesting that SAA directly induces PTX3. CONCLUSION: Our data suggest that SAA plays a role in the proinflammatory and immune responses in rheumatoid synovium by inducing PTX3. We provide the first evidence that the acute-phase reactant SAA, which is produced systemically by hepatocytes, perpetuates the rheumatoid inflammatory processes by inducing another proinflammatory molecule, PTX3, locally in rheumatoid synovial tissues.
Assuntos
Artrite Reumatoide/metabolismo , Proteína C-Reativa/metabolismo , Osteoartrite/metabolismo , Proteína Amiloide A Sérica/farmacologia , Componente Amiloide P Sérico/metabolismo , Membrana Sinovial/efeitos dos fármacos , Artrite Reumatoide/patologia , Proteína C-Reativa/antagonistas & inibidores , Proteína C-Reativa/genética , Inibidores Enzimáticos/farmacologia , Regulação da Expressão Gênica/efeitos dos fármacos , Inativação Gênica , Humanos , Quinases de Proteína Quinase Ativadas por Mitógeno/antagonistas & inibidores , NF-kappa B/antagonistas & inibidores , Osteoartrite/patologia , RNA Mensageiro/metabolismo , RNA Interferente Pequeno/farmacologia , Receptores de Formil Peptídeo/genética , Receptores de Formil Peptídeo/metabolismo , Receptores de Lipoxinas/genética , Receptores de Lipoxinas/metabolismo , Proteínas Recombinantes , Componente Amiloide P Sérico/antagonistas & inibidores , Componente Amiloide P Sérico/genética , Membrana Sinovial/metabolismo , Membrana Sinovial/patologia , TransfecçãoRESUMO
BACKGROUND: Monosodium urate (MSU) has been shown to promote inflammasome activation and interleukin-1ß (IL-1ß) secretion in monocyte/macrophages, but the cellular pathway and nod-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome activation in synovial tissues, remain elusive. In this study, we investigated the effects of MSU on synovial fibroblasts to elucidate the process of MSU-mediated synovial inflammation. METHODS: Human synovial fibroblasts were stimulated with MSU in the presence or absence of serum amyloid A (SAA). The cellular supernatants were analyzed by immunoblotting using anti-IL-1ß or anti-caspase-1 antibodies. IL-1ß or NLRP3 mRNA expressions were analyzed by real-time PCR or reverse transcription-PCR (RT-PCR) method. RESULTS: Neither SAA nor MSU stimulation resulted in IL-1ß or interleukin-1α (IL-1α) secretions and pro-IL-1ß processing in synovial fibroblasts. However, in SAA-primed synovial fibroblasts, MSU stimulation resulted in the activation of caspase-1 and production of active IL-1ß and IL-1α. The effect of SAA on IL-1ß induction was impaired in cells by silencing NLRP3 using siRNA or treating with caspase-1 inhibitor. In addition, SAA induced the secretion of cathepsin B and NLRP3 mRNA expression in synovial fibroblasts. CONCLUSIONS: Our data demonstrate that exposure of human synovial fibroblasts to SAA promotes MSU-mediated caspase-1 activation and IL-1ß secretion in the absence of microbial stimulation. These findings provide insight into the molecular processes underlying the synovial inflammatory condition of gout.