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Neuroimmunomodulation. 2014;21(6):331-7. doi: 10.1159/000357811. Epub 2014 Mar 8.

Investigations into the role of 26S proteasome non-ATPase regulatory subunit 13 in neuroinflammation.

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1
Department of Neurology, First Affiliated Hospital of Jinan University, Guangzhou, PR China.

Abstract

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 (IκBα) 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 IκBα 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 E2.

CONCLUSIONS:

PSMD13 gene silencing suppressed the production of proinflammatory mediators by modulating ubiquitin-proteasome system-mediated neuroinflammation via the downregulation of IκBα degradation and NF-κB activation in LPS-stimulated BV2 microglia. PSMD13 gene knockdown may have therapeutic implications for the treatment of neuroinflammatory disorders.

PMID:
24642793
DOI:
10.1159/000357811
[Indexed for MEDLINE]
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