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http://purl.uniprot.org/citations/31751919http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/31751919http://www.w3.org/2000/01/rdf-schema#comment"

Objective

The neuronal wiskott-aldrich syndrome protein (N-WASP) is a member of the wiskott-aldrich syndrome protein (WASP) family. N-WASP plays a vital role in promoting cell migration, receptor signaling and immune inflammatory responses. This study aimed to observe the changes in the expression of inflammatory factors and involving pathways after N-WASP knockdown in human gingival fibroblasts (HGFs).

Design

Gingival inflammatory condition of N-WASP knockout mice was evaluated by H&E staining. N-WASP in HGFs was knockdown by siRNA and the best knockdown efficiency was determined by qRT-PCR and immunofluorescence. The mRNA levels of interleukin (IL)-6, IL-8, C-C motif ligand 2 (CCL2), superoxide dismutase 2 (SOD2) and prostaglandin endoperoxide synthase 2 (PTGS2) were evaluated by qRT-PCR after N-WASP knockdown with or without mitogen-activated protein kinase (MAPK) and nuclear factor-κB (NF-κB) inhibitors. The protein levels of IL-6, IL-8 and CCL2 were assessed by ELISA. Western blotting was used to detect the activation of NF-κB and MAPK signaling pathways.

Results

Gingival tissue from N-WASP knockout mice exhibited an inflammatory reaction. The expression of IL-6, IL-8, CCL2, SOD2 and PTGS2 was significantly upregulated after N-WASP knockdown in HGFs for 6, 24 and 48 h, except for the SOD2 at 6 h. N-WASP knockdown significantly activated the signaling pathways of NF-κB and MAPK. The inhibitors of p65, p38, ERK and JNK clearly decreased IL-6, IL-8, CCL2, SOD2 and PTGS2 expression after N-WASP knockdown.

Conclusion

These data indicated that N-WASP deficiency in HGFs increases the production of inflammatory cytokine and is regulated via NF-κB and MAPK signaling pathways."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.org/dc/terms/identifier"doi:10.1016/j.archoralbio.2019.104605"xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/author"Kang W."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/author"Wang Y."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/author"Ge S."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/author"Shang L."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/author"Song A."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/date"2020"xsd:gYear
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/name"Arch Oral Biol"xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/pages"104605"xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/title"N-WASP knockdown upregulates inflammatory cytokines expression in human gingival fibroblasts."xsd:string
http://purl.uniprot.org/citations/31751919http://purl.uniprot.org/core/volume"110"xsd:string
http://purl.uniprot.org/citations/31751919http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/31751919
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