TY - JOUR
AU - Tao, Enxiang
AB - Objective: To investigate 26S proteasome non-ATPase regulatory subunit 13 (PSMD13) gene silencing as a potential treatment for neuroinflammatory disorders via regulation of microglial activation and production of inflammatory mediators. Methods: RNA interference was used to knockdown PSMD13 gene expression, followed by inhibitors of κB (IκBa) protein degradation and nuclear factor κB (NF-κB) activity measurement in lipopolysaccharide (LPS)-stimulated BV2 microglia. Nitrite (Griess) assay, reporter gene assay, enzyme-linked immunosorbent assay and Western blot were used to investigate the role of PSMD13 in microglial activation and inflammation. Results: PSMD13 gene knockdown significantly reduced IκBa degradation and NF-κB activation in LPS-stimulated murine BV2 microglia. It also decreased the production of LPS-induced proinflammatory mediators, such as inducible nitric oxide synthase, nitric oxide, cyclooxygenase-2 and prostaglandin E<sub>2</sub>. Conclusions: PSMD13 gene silencing suppressed the production of proinflammatory mediators by modulating ubiquitin-proteasome system-mediated neuroinflammation via the downregulation of IκBa degradation and NF-κB activation in LPS-stimulated BV2 microglia. PSMD13 gene knockdown may have therapeutic implications for the treatment of neuroinflammatory disorders.
TI - Investigations into the Role of 26S Proteasome Non-ATPase Regulatory Subunit 13 in Neuroinflammation
JF - Neuroimmunomodulation
DO - 10.1159/000357811
DA - 2014-01-01
UR - https://www.deepdyve.com/lp/karger/investigations-into-the-role-of-26s-proteasome-non-atpase-regulatory-XrmrkmRsJF
SP - 331
EP - 337
VL - 21
IS - 6
DP - DeepDyve
ER -